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Acute Respiratory Distress Syndrome

Asta Literature Retrieval: Pathophysiology and clinical mechanisms of Acute Respiratory Distress Syndrome. Core disease mechanisms, molecular an...

2026-08-08
Asta MONDO:0006502 Model: Asta Scientific Corpus Retrieval 20 citations

Asta Literature Retrieval: Pathophysiology and clinical mechanisms of Acute Respiratory Distress Syndrome. Core disease mechanisms, molecular an...

This report is retrieval-only and is generated directly from Asta results.

  • Papers retrieved: 20
  • Snippets retrieved: 20

Relevant Papers

[1] Lung regeneration: diverse cell types and the therapeutic potential

  • Authors: Yutian Chen, Zhen Li, Gaili Ji, Shaochi Wang, Chunheng Mo et al.
  • Year: 2024
  • Venue: MedComm
  • URL: https://www.semanticscholar.org/paper/0fbe00de4b129b66ffcc63fd4298d45dc0352a8c
  • DOI: 10.1002/mco2.494
  • PMID: 38405059
  • PMCID: 10885188
  • Citations: 30
  • Summary: A review of the molecular and cellular mechanisms of lung regeneration, drug development, and clinical trials provides a reference for further research on the molecular and cellular mechanisms of lung regeneration, drug development, and clinical trials.
  • Evidence snippets:
  • Snippet 1 (score: 0.502) > Abstract Lung tissue has a certain regenerative ability and triggers repair procedures after injury. Under controllable conditions, lung tissue can restore normal structure and function. Disruptions in this process can lead to respiratory system failure and even death, causing substantial medical burden. The main types of respiratory diseases are chronic obstructive pulmonary disease (COPD), idiopathic pulmonary fibrosis (IPF), and acute respiratory distress syndrome (ARDS). Multiple cells, such as lung epithelial cells, endothelial cells, fibroblasts, and immune cells, are involved in regulating the repair process after lung injury. Although the mechanism that regulates the process of lung repair has not been fully elucidated, clinical trials targeting different cells and signaling pathways have achieved some therapeutic effects in different respiratory diseases. In this review, we provide an overview of the cell type involved in the process of lung regeneration and repair, research models, and summarize molecular mechanisms involved in the regulation of lung regeneration and fibrosis. Moreover, we discuss the current clinical trials of stem cell therapy and pharmacological strategies for COPD, IPF, and ARDS treatment. This review provides a reference for further research on the molecular and cellular mechanisms of lung regeneration, drug development, and clinical trials.

[2] Acute respiratory distress syndrome (ARDS): from mechanistic insights to therapeutic strategies

  • Authors: Rongli Xie, Dan Tan, Boke Liu, Guohui Xiao, Fangchen Gong et al.
  • Year: 2025
  • Venue: MedComm
  • URL: https://www.semanticscholar.org/paper/97d3e572d53d14edaa3fdb78fe49b51047c7aabc
  • DOI: 10.1002/mco2.70074
  • PMID: 39866839
  • PMCID: 11769712
  • Citations: 33
  • Influential citations: 1
  • Summary: The pathogenesis and treatment methods of affected organs, including 2019 coronavirus disease (COVID‐19)‐related pneumonia, drowning, trauma, blood transfusion, severe acute pancreatitis, and sepsis are discussed.
  • Evidence snippets:
  • Snippet 1 (score: 0.491) > Acute respiratory distress syndrome (ARDS) is a clinical syndrome of acute hypoxic respiratory failure caused by diffuse lung inflammation and edema. The mortality rate is high in ARDS patients and is related to the severity of the patient's condition. 1 ARDS can be precipitated by intrapulmonary factors (pneumonia, aspiration, etc.) or extrapulmonary factors (severe acute pancreatitis [SAP], sepsis, trauma, etc.), which can lead to severe hypoxemia, decreased lung compliance, increased arteriovenous shunts, and increased physiological dead space. 4][5] Each revision of the definition, in response to new research findings and clinical concepts, is intended to provide a definition that consistently and accurately identifies patients. The pathophysiology of ARDS is complex and involves the activation and dysregulation of multiple overlapping and interacting pathways of systemic inflammation and coagulation, including the respiratory, circulatory, and immune systems. In general, the treatment of inflammatory injuries is a coordinated process that involves the downregulation of proinflammatory pathways and the upregulation of anti-inflammatory pathways. Owing to differences in etiology and inducement, there is heterogeneity in the clinical syndrome. In recent years, foundation medicine, radiology, immunology, and other disciplines have increasingly recognized and incorporated phenotype recognition. > ARDS is a highly heterogeneous disease with different etiologies, different inflammatory phenotypes and different histomorphologic characteristics, which leads to relatively slow progress in the treatment of ARDS. Individualized medical approaches to the etiology of ARDS can improve the identification of ARDS phenotypes, which should contribute to a better understanding of its pathophysiological mechanisms and differences between patients. In this review, we discuss the current understanding of the structural features and changes in the lung function of ARDS patients. We further discuss the pathogenesis and treatment methods of affected organs according to their different causes.

[3] A practical approach to adult acute respiratory distress syndrome

  • Authors: C. Manthous
  • Year: 2010
  • Venue: Indian Journal of Critical Care Medicine : Peer-reviewed, Official Publication of Indian Society of Critical Care Medicine
  • URL: https://www.semanticscholar.org/paper/affa7b3f3d93c8318e50fb89eabdce8c86696a23
  • DOI: 10.4103/0972-5229.76084
  • PMID: 21572751
  • PMCID: 3085221
  • Citations: 4
  • Summary: The clinical features and how pathophysiology informs the evidence-based management of ARDS are reviewed, which shows how the disease has carried a very high mortality.
  • Evidence snippets:
  • Snippet 1 (score: 0.489) > Acute respiratory distress syndrome (ARDS) is a common disease encountered in hospitalized adult patients that, historically, has carried a very high mortality. This article reviews the clinical features and how pathophysiology informs the evidence-based management of ARDS.

[4] Genetic and Multi‐Omics Insights Into Monocyte Pantothenate‐Mediated Protection in Acute Respiratory Distress Syndrome

  • Authors: Yang Wang, Hongyu Sun, Fengying Liang, Y. Qian, Yuanyuan Wang et al.
  • Year: 2025
  • Venue: Journal of Cellular and Molecular Medicine
  • URL: https://www.semanticscholar.org/paper/475776c4266e5af912ab92f23bff48fd16d5fd2c
  • DOI: 10.1111/jcmm.70812
  • PMID: 41059665
  • PMCID: 12505201
  • Citations: 4
  • Summary: This study uses Mendelian randomisation, multi‐omics and machine learning approaches to provide novel insights into the pathogenesis of ARDS and its potential therapeutic strategies targeting monocyte metabolism and function.
  • Evidence snippets:
  • Snippet 1 (score: 0.467) > Acute respiratory distress syndrome (ARDS) is a severe and life-threatening condition characterised by rapid onset of widespread inflammation and increased permeability of the alveolar-capillary barrier, leading to impaired gas exchange and respiratory failure [1,2]. Despite advances in supportive care, including lung-protective ventilation strategies and neuromuscular blockade, the mortality rate for ARDS remains high, ranging from 30% to 45% [3]. This persistent mortality burden highlights the critical need for a deeper understanding of the underlying pathophysiology to inform the development of more effective therapeutic interventions. > Emerging evidence suggests that metabolic factors may play a crucial role in the pathogenesis of ARDS, though the precise mechanisms remain incompletely understood [4,5]. Alterations in cellular metabolism, including impaired energy production, oxidative stress and dysregulated signalling pathways, have been implicated in the initiation and progression of ARDS [6,7]. Furthermore, metabolic disturbances, such as hyperglycemia, dyslipidaemia and mitochondrial dysfunction, have been associated with worse clinical outcomes in ARDS patients [8][9][10][11]. However, the specific metabolic pathways and mediators involved in the development and resolution of ARDS remain poorly defined [12]. Continued research is necessary to elucidate this complex interplay between metabolism and the pathogenesis of ARDS, which may lead to the identification of novel therapeutic targets and the development of more personalised treatment strategies. > In this study, we aim to investigate the causal relationship between plasma metabolites, immune cell profiles and the risk of ARDS using Mendelian randomisation (MR) analysis. We integrate single-cell sequencing and transcriptomic data to explore the potential mechanisms underlying these associations. Additionally, we employ machine learning approaches to evaluate the predictive performance of a comprehensive set of risk factors for ARDS development. By elucidating the causal pathways and underlying biological mechanisms linking these metabolic and immune factors to ARDS, our research is expected to provide important insights into the pathogenesis of this devastating syndrome.

[5] Obesity promotes ARDS by modulating ceramide transfer protein-ceramide pathway and exacerbating oxidative stress/apoptosis in alveolar macrophages

  • Authors: Yichan Ao, Jingyue Ma, Xiangyu Hou, Hongbin Li, Zhiqiao Wang et al.
  • Year: 2025
  • Venue: Cellular and Molecular Life Sciences: CMLS
  • URL: https://www.semanticscholar.org/paper/23ee5a5309e9b3ceefad8175244fc04a35dbb765
  • DOI: 10.1007/s00018-025-05706-9
  • PMID: 40537702
  • PMCID: 12179041
  • Citations: 4
  • Summary: In vivo and in vitro studies indicated that obesity-induced downregulation of CERT reduced Cer transport, increased Cer levels, and aggravated ARDS through elevated ROS production and apoptosis, highlighting CERT may represent a promising therapeutic target for managing ARDS in individuals with obesity.
  • Evidence snippets:
  • Snippet 1 (score: 0.461) > Acute respiratory distress syndrome (ARDS) is a common critical condition characterized by acute respiratory distress and progressive hypoxemia, with its pathogenesis not yet fully understood. Approximately 10.4% of patients in intensive care units (ICUs) develop ARDS, a condition associated with high morbidity and mortality [1]. Obesity, a systemic chronic low-grade inflammatory state, is a wellestablished risk factor for various respiratory diseases [2]. Notably, obesity has been identified as an independent risk factor for the development of ARDS in ICU patients, with the risk nearly doubling in obese individuals [3][4][5]. Despite growing evidence that obesity increases susceptibility to ARDS and worsens disease severity, the mechanisms by which obesity contributes to the onset and progression of ARDS remain poorly understood. Therefore, animal models and basic research that reflect clinical characteristics are crucial for elucidating the specific mechanisms linking obesity and ARDS, potentially laying the groundwork for improving ARDS treatment outcomes [6][7][8][9]. > Multiple studies have demonstrated that "omics" strategies significantly contribute to understanding the pathophysiological pathways underlying diseases. Proteins, as the primary executors of biological functions, represent the final products of genetic information, while metabolites are essential components of cellular processes, participating in enzyme-catalyzed reactions critical for cell function. Quantitative proteomics allows for detailed characterization of pathogenic biochemical processes by measuring protein levels and their regulatory chemical modifications [10]. Additionally, metabolomics provides a wealth of information that strongly predicts phenotypic outcomes [11]. In recent years, these strategies have become valuable tools for exploring the etiology and mechanisms of obesity-related diseases [12][13][14][15]. In acute lung injury (ALI) or ARDS, various candidate biomarkers have been identified through the assessment of protein expression in lung tissues [16][17][18]. Moreover, integrated proteomics and metabolomics analyses have facilitated the identification of mechanisms relevant to drugs aimed at preventing or ameliorating ALI/ARDS [19]. However, specific changes in the protein and metabolite profiles associated with ARDS in HFD mice have yet to be characterized.

[6] Evolution of multiple omics approaches to define pathophysiology of pediatric acute respiratory distress syndrome

  • Authors: Jane E Whitney, In‐Hee Lee, Ji-Won Lee, S. Kong
  • Year: 2022
  • Venue: eLife
  • URL: https://www.semanticscholar.org/paper/6d82effd3fff4275e47d52ecd0b92ee996e2ac37
  • DOI: 10.7554/eLife.77405
  • PMID: 35913450
  • PMCID: 9342956
  • Citations: 5
  • Summary: Novel profiling methods such as scRNA-seq, which permits more comprehensive, unbiased evaluation of pathophysiological mechanisms across tissue and cell types, should be employed to investigate the molecular mechanisms of PRDS toward the goal of identifying targeted therapies.
  • Evidence snippets:
  • Snippet 1 (score: 0.453) > Pediatric acute respiratory distress syndrome (PARDS), though both common and deadly in critically ill children, lacks targeted therapies. The development of effective pharmacotherapies has been limited, in part, by lack of clarity about the pathobiology of pediatric ARDS. Epithelial lung injury, vascular endothelial activation, and systemic immune activation are putative drivers of this complex disease process. Prior studies have used either hypothesis-driven (e.g., candidate genes and proteins, in vitro investigations) or unbiased (e.g., genome-wide association, transcriptomic, metabolomic) approaches to predict clinical outcomes and to define subphenotypes. Advances in multiple omics technologies, including genomics, transcriptomics, proteomics, and metabolomics, have permitted more comprehensive investigation of PARDS pathobiology. However, omics studies have been limited in children compared to adults, and analyses across multiple tissue types are lacking. Here, we synthesized existing literature on the molecular mechanism of PARDS, summarized our interrogation of publicly available genomic databases to determine the association of candidate genes with PARDS phenotypes across multiple tissues and cell types, and integrated recent studies that used single-cell RNA sequencing (scRNA-seq). We conclude that novel profiling methods such as scRNA-seq, which permits more comprehensive, unbiased evaluation of pathophysiological mechanisms across tissue and cell types, should be employed to investigate the molecular mechanisms of PRDS toward the goal of identifying targeted therapies.

[7] Classic Signaling Pathways in Alveolar Injury and Repair Involved in Sepsis-Induced ALI/ARDS: New Research Progress and Prospect

  • Authors: Wenli Li, Duo Li, Yuansen Chen, Halidan Abudou, Haiwang Wang et al.
  • Year: 2022
  • Venue: Disease Markers
  • URL: https://www.semanticscholar.org/paper/4268a462890d48f33ce3908d40f66ecb9f3dd801
  • DOI: 10.1155/2022/6362344
  • PMID: 35726235
  • PMCID: 9206211
  • Citations: 127
  • Influential citations: 3
  • Summary: The signaling pathways related to alveolar injury and repair in sepsis-induced ALI/ARDS and their latest research progress include the NF-κB, JAK2/STAT3, mitogen-activated protein kinase (MAPK), mTOR, and Notch signaling pathways.
  • Evidence snippets:
  • Snippet 1 (score: 0.449) > Sepsis is a common critical clinical disease with high mortality that can cause approximately 10 million deaths worldwide each year. Acute lung injury (ALI) or acute respiratory distress syndrome (ARDS) is a common clinical complication of sepsis, which occurs primarily as diffuse alveolar injury, hypoxemia, and respiratory distress. The mortality rate of ALI/ARDS is as high as 30%-40%, which greatly endangers human health. Due to the unclear pathogenesis of ALI/ARDS, its treatment is still a worldwide problem. At present, clinical treatment mainly relies on lung-protective ventilation, prone position ventilation, and fluid management. However, there is a lack of effective and specific treatment measures. In recent years, domestic and foreign scholars have committed to basic research on ALI/ARDS, trying to further clarify its pathogenesis and find new targets and methods for the treatment of ALI/ARDS. In this review, we summarize the signaling pathways related to alveolar injury and repair in sepsis-induced ALI/ARDS and their latest research progress. They include the NF-κB, JAK2/STAT3, mitogen-activated protein kinase (MAPK), mTOR, and Notch signaling pathways. Understanding the molecular mechanisms of these signaling pathways in sepsis-induced ALI/ARDS may provide new targets and ideas for the clinical treatment of this disease.

[8] Acute Respiratory Failure: Pathophysiological Basis From A Multidisciplinary Clinical Approach

  • Authors: R. Castillo
  • Year: 2015
  • Venue: The Open Respiratory Medicine Journal
  • URL: https://www.semanticscholar.org/paper/f4537439b4e55e4efb383f03c5c3f561d9fcedf8
  • DOI: 10.2174/1874306401509010081
  • PMID: 26312098
  • PMCID: 4541451
  • Citations: 1
  • Summary: The evidence strongly supports its use in patients with chronic obstructive pulmonary disease (COPD) exacerbation, patients with acute cardiogenic pulmonary edema and immunosuppressed patients, and patients with hypoxemic and hypercapnic failure.
  • Evidence snippets:
  • Snippet 1 (score: 0.443) > Acute Respiratory Failure: Pathophysiological Basis from a Multidisciplinary Clinical Approach > Acute Respiratory Failure (ARF) is a syndrome characterized by the inability of the respiratory system to maintain adequate arterial O2 and CO2 levels according to the demands of cellular metabolism. ARF may be caused by the failure of the exchanger, lung, organ or pump, or failure of the respiratory muscles. ARF can be classified by the dysfunctional element or the evolution time when the condition occurs. > Acute lung injury/acute respiratory distress syndrome (ALI/ARDS) is the most important cause of adults hipoxemic respiratory failure, which results from multiple clinical factors such as sepsis or trauma [1]. Although the main cause was clinically resolved, the mechanism that determines the progression may persist and lead to complications. > However, It is demonstrated that the clinical causes of respiratory failure increase the intensive care units (ICU) stay, the sanitary cost and the global mortality [2]. For this reason, multidisciplinary and pathophysiological focus on respiratory failure is necessary for the management of these patients. > The application of non-invasive mechanical ventilation (NIMV) has acquired major relevance in the last few years in the management of ARF, in patients with hypoxemic and hypercapnic failure. The main advantage of NIMV compared to invasive mechanical ventilation is that it can be used earlier outside ICU. The evidence strongly supports its use in patients with chronic obstructive pulmonary disease (COPD) exacerbation, patients with acute cardiogenic pulmonary edema and immunosuppressed patients. > This issue is focused on the mechanism associated with ARF, some clinical syndromes, and the pathophysiological bases for the use of ventilatory strategies, with a multidisciplinary approach.

[9] Messenger RNA sequencing reveals similar mechanisms between neonatal and acute respiratory distress syndrome

  • Authors: H. Mei, Yuheng Zhang, Chun-zhi Liu, Yayu Zhang, Chunli Liu et al.
  • Year: 2017
  • Venue: Molecular Medicine Reports
  • URL: https://www.semanticscholar.org/paper/663e1561706e158cfc150ce2f69d0b6a184888e4
  • DOI: 10.3892/mmr.2017.7891
  • PMID: 29115600
  • PMCID: 5780146
  • Citations: 8
  • Summary: Using peripheral blood obtained from mature infants with and without NRDS and in tandem with mRNA sequencing, the present study identified that, while cell cycle regulation and alveolar surfactants serve a role in deterring the further onset of NRDS, innate and pathogen-induced responses of the immune system are among the most important factors in the pathology.
  • Evidence snippets:
  • Snippet 1 (score: 0.441) > Neonatal respiratory distress syndrome (NRDS), also termed hyaline membrane disease, is one of the most prevalent causes of morbidity and mortality in newborns (1). The oxygen diffusion efficiency through the alveoli-capillary exchange barrier is impacted by the dysregulation of numerous factors, leading to the pathophysiology of NRDS (2). Cellular stress at the gas-blood level is associated with alterations in alveolar surfactant proteins (3) and the upregulation of numerous innate immune responses of pro-inflammatory cytokines to foreign challenges (4). A lack of surfactant may drive the pathogenesis towards NRDS, while surfactant replacement therapy may mitigate symptoms of the disease by decreasing the surface tension of alveoli and facilitating their inflation (5,6). However, surfactant serves an additional role in immunological processes. A recent study demonstrated that applying clinical surfactant for patients led to a stronger response to challenges from foreign microbiota (7). Additionally, animal-derived surfactant applied for clinical use in humans has been demonstrated to be of use against lung pathogens and to mediate excess host damage from neutrophils (8). Therefore, it may be hypothesized that mechanisms that mechanisms of NRDS involving surfactant exert additional functions to promoting alveolar inflation. > Acute respiratory distress syndrome (ARDS) is a clinical phenotype precipitated by the manifestation of a severe form of lung injury due to numerous lung insults (9). The pathophysiological manifestation of ARDS is derived from a cascade that is triggered by the complex combination of risk factors, including asthma, sepsis, pneumonia, increased neutrophil presence in the lungs and other variables; accumulation of these numerous systemic factors forms the pathological endpoint of ARDS (10). > The present study used peripheral blood obtained from infants with (n=4) or without (n=2) NRDS in tandem with mRNA-sequencing (mRNA-seq) analysis to reveal various factors involved in the mechanisms of NRDS, and to compare onset mechanisms between NRDS and ARDS.

[10] NR4A1 Promotes LPS-Induced Acute Lung Injury through Inhibition of Opa1-Mediated Mitochondrial Fusion and Activation of PGAM5-Related Necroptosis

  • Authors: Pingjun Zhu, Junyan Wang, Wenjuan Du, Jun Ren, Ying Zhang et al.
  • Year: 2022
  • Venue: Oxidative Medicine and Cellular Longevity
  • URL: https://www.semanticscholar.org/paper/7551d2b7ca961dd3d6f1e79086321b021411941d
  • DOI: 10.1155/2022/6638244
  • PMID: 35222801
  • PMCID: 8881136
  • Citations: 29
  • Summary: The data identified NR4A1 as a novel regulator of LPS‐related acute lung injury through regulation of mitochondrial fusion and necroptosis, indicating therapeutic promises of targeting NR4A1 in the treatment of acute lung injury in clinical practice.
  • Evidence snippets:
  • Snippet 1 (score: 0.440) > Acute respiratory distress syndrome (ARDS), a diffused injury of the lung parenchyma evoked by pathological stresses including severe infection, anoxia, ischemia, trauma, and surgery [1,2], is deemed one of the most common refractory complications with high mortality and mortality in critically ill patients [3,4]. To date, effective therapy for ARDS is still lacking. Ample experimental findings have unveiled the pathogenesis of ARDS with beneficial effects from pharmacological and mechanical conditioning strategies [5]. In particular, a number of mechanisms have been Oxidative Medicine and Cellular Longevity suggested to contribute to ARDS including oxidative stress, inflammation response, and immunomodulatory disorders [6][7][8]. A better understanding of the interplay among these pathological factors should help to unveil novel therapeutic strategies for acute lung injury and clinical outcomes in patients with ARDS. > Given the important role of mitochondria in energy metabolism through consumption of nutrient and oxygen by way of tricarboxylic acid cycle and oxidative phosphorylation (OXPHOS), mitochondria serve as the powerhouse in cells [9]. Besides, a range of cellular physiological processes such as oxidative stress, calcium regulation, signaling transduction, cell movement, growth, proliferation, and death are controlled by mitochondria, especially in respiratory diseases including but not limited to ARDS. Mitochondrialderived reactive oxygen species (ROS) has aroused considerable attention due to its dual regulatory role in ARDS [10]. In lipopolysaccharide-(LPS-) induced acute lung injury, mitochondrial APT production is reduced whereas levels of ROS are elevated, because of neutrophil accumulation in lung tissues [11]. Furthermore, mitochondrial ROStriggered oxidative damage as well as mitochondrial apopto-sis is noted in kidney tissues following LPS challenge [12]. Another independent study in a model of endotoxininduced ARDS revealed a connection between mitochondrial bioenergetic dysfunction and impaired pulmonary ventilation [13]. These findings indicate a role of mitochondrial dysfunction in acute lung injury although precise molecular mechanisms are not fully understood.

[11] Candidate genes and pathogenesis investigation for sepsis-related acute respiratory distress syndrome based on gene expression profile

  • Authors: Min Wang, Jingjun Yan, Xingxing He, Q. Zhong, Cheng-ye Zhan et al.
  • Year: 2016
  • Venue: Biological Research
  • URL: https://www.semanticscholar.org/paper/88c3aefab1fe6d50848633dff472cda669b57ae2
  • DOI: 10.1186/s40659-016-0085-4
  • PMID: 27090785
  • PMCID: 4835843
  • Citations: 22
  • Influential citations: 1
  • Summary: Genes including CCNB1, CCNB2 and TOP2A, as well as transcription factors like FOXM1 might be used as the novel gene therapy targets for sepsis related ARDS.
  • Evidence snippets:
  • Snippet 1 (score: 0.439) > Acute respiratory distress syndrome (ARDS) is a potentially devastating form of acute inflammatory lung injury as well as a major cause of acute respiratory failure. Although researchers have made significant progresses in elucidating the pathophysiology of this complex syndrome over the years, the absence of a universal detail disease mechanism up until now has led to a series of practical problems for a definitive treatment. This study aimed to predict some genes or pathways associated with sepsis-related ARDS based on a public microarray dataset and to further explore the molecular mechanism of ARDS. A total of 122 up-regulated DEGs and 91 down-regulated differentially expressed genes (DEGs) were obtained. The up- and down-regulated DEGs were mainly involved in functions like mitotic cell cycle and pathway like cell cycle. Protein–protein interaction network of ARDS analysis revealed 20 hub genes including cyclin B1 (CCNB1), cyclin B2 (CCNB2) and topoisomerase II alpha (TOP2A). A total of seven transcription factors including forkhead box protein M1 (FOXM1) and 30 target genes were revealed in the transcription factor-target gene regulation network. Furthermore, co-cited genes including CCNB2-CCNB1 were revealed in literature mining for the relations ARDS related genes. Pathways like mitotic cell cycle were closed related with the development of ARDS. Genes including CCNB1, CCNB2 and TOP2A, as well as transcription factors like FOXM1 might be used as the novel gene therapy targets for sepsis related ARDS.

[12] A comprehensive systematic review of the phenotypes and their role in improving medications and clinical results in the acute respiratory distress syndrome: exploring the potential of personalized therapy

  • Authors: E. R. Surabhi, Devanshu J. Patel, Asha Kademane, Pradeep Nirala
  • Year: 2024
  • Venue: Multidisciplinary Reviews
  • URL: https://www.semanticscholar.org/paper/82200075790bb220d807d97ca7f9f49d62449341
  • DOI: 10.31893/multirev.2023ss006
  • Summary: The significance of customizing research trials to the exact stage of lung damage that patients are experiencing, as well as premature treatment and preventive intervention and developed ARDS therapy are discussed.
  • Evidence snippets:
  • Snippet 1 (score: 0.438) > The Acute Respiratory Distress Syndrome (ARDS) is a disorder that can be severe and it is characterized by severe breathing difficulties, such as the various clinical risk factors, lung injury mechanisms, microbiological aspects and biological factors. The current systematic review intends to investigate the phenotypic diversity in ARDS and the possibility of individualized treatment in improving clinical outcomes. In the field of molecular phenotyping, biomarker panels show promise as useful tools for identifying patients who are at risk of developing ARDS, diagnosing the disease, assisting in risk assessment and allowing for ongoing observation. The hyper-inflammatory subphenotype is associated with diseases including metabolic acidosis, shock and worse clinical outcomes. Biologic phenotypes are taken into consideration, such as gene expression, common causal microbiologic infections and plasma protein biomarkers. This review underlines the variations in etiology, clinical manifestations and treatment responses for the diverse phenotypes, including subtypes of direct and indirect lung damage. We will talk about the significance of customizing research trials to the exact stage of lung damage that patients are experiencing, as well as premature treatment and preventive intervention and developed ARDS therapy. Customized therapy can become a reality as a result of improved clinical trial design and execution brought by a deeper comprehension of the interactions between various factors in ARDS.

[13] Single-cell analysis reveals dysregulated inflammatory response in peripheral blood immunity in patients with acute respiratory distress syndrome

  • Authors: Jingjia Mo, Yanli Yang, Jihua Feng, Yanhua Lei, Suhong Huang et al.
  • Year: 2023
  • Venue: Frontiers in Cell and Developmental Biology
  • URL: https://www.semanticscholar.org/paper/38d0e7e914d64151dc384d2d068b30f351473825
  • DOI: 10.3389/fcell.2023.1199122
  • PMID: 37283946
  • PMCID: 10239863
  • Citations: 7
  • Summary: The composition of cells involved in the main peripheral circulation differs in patients with ARDS with different etiologies, and a significant enhancement of the oxidative stress response was observed in the neutrophil subpopulation.
  • Evidence snippets:
  • Snippet 1 (score: 0.432) > Introduction: Acute respiratory distress syndrome (ARDS) remains a major clinical challenge for patients in intensive care units. Determining the differential mechanisms underlying ARDS with different etiologies is a key goal to improve the effectiveness of ARDS therapy. Despite growing evidence that different immune cell types are involved in ARDS, the role of altered immune cell subpopulations in disease progression is unelucidated. Methods: In this study, we combined scRNA-seq and bulk-level sequencing to analyze the transcriptomes of peripheral blood mononuclear cells from healthy volunteers and patients with septic ARDS (sep-ARDS) and pneumonic ARDS (PNE-ARDS). Results: Our data revealed differential alterations at the cellular and molecular levels and within biological signaling pathways in ARDS with different etiologies. The dynamics of neutrophils, macrophages (Macs), classical dendritic cells (cDCs), myeloid-derived suppressive cells (MDSCs), and CD8+ T cells varied significantly among groups of different samples, with neutrophils and cDCs at higher, and Macs at significantly lower, amounts in the patients with sep-ARDS. Furthermore, MDSCs were highly enriched only in the sep-ARDS patients, whereas a higher abundance of CD8+ T cells was observed in patients with PNE-ARDS. In addition, these cell subpopulations were found to be significantly involved in apoptosis, inflammatory, and immune-related pathways. In particular, a significant enhancement of the oxidative stress response was observed in the neutrophil subpopulation. Conclusion: Our study shows that the composition of cells involved in the main peripheral circulation differs in patients with ARDS with different etiologies. Studying the role and mechanism of action of these cells during ARDS will provide new opportunities for the treatment of this condition.

[14] Advancement in Precision Medicine and Recommendation System for Clinical Trials Using Deep Learning Methods

  • Authors: A.P.Ponselvakumar, S. Anandamurugan, K.Logeswaran, S.Nivashini, S.K.Showentharya et al.
  • Year: 2021
  • Venue: IOP Conference Series: Materials Science and Engineering
  • URL: https://www.semanticscholar.org/paper/09c40cae147b54bbb86db9825a1c96299acedbc5
  • DOI: 10.1088/1757-899X/1055/1/012110
  • Citations: 6
  • Influential citations: 1
  • Summary: Both combination of recommendation system along with deep learning quality of precision healthcare achieved to patients are revealed.
  • Evidence snippets:
  • Snippet 1 (score: 0.432) > The following paper [25] briefly talks about biomarkers which play a significant role within the treatment of respiratory functionalities. It is stated that over 10% of patients hospitalized in critical care are affected by Acute Lung Injury. The most intense type of ALI is Acute respiratory distress syndrome (ARDS) in which 40% fatality rate is observed. The contribution of biomarkers to the pathophysiology of ARDS is considerably very less. Nevertheless, a major problem is that ARDS is such a diverse, multi-factorial, termination condition that the techniques for "lumping and splitting" are severe. > However, the appliance of network biology to ARDS is made possible with the help of human genome sequencing and the provision of improved techniques for the analysis purpose of transcription to mRNA (gene expression), and also due to the development of sensitive immunoassays. In the field of molecular phenotypic is to identify the patients who at the danger to develop ARDS, biomarker panels have gained prospective applications. This composite disease continues to be serious and deadly event even though the process of dealing and controlling of ARDS has been developed. Monoclonal antibodies (anti-TNF) and TNFR fusion protein have given uncompromising results. However, with the advancement in the techniques of mechanical ventilation, a neuromuscular blocker has shown some positive result, and somatic cell therapy is being well developed. In the future, it is expected that this could give logical remedial targets, and eventually improve clinical care since the comprehension role of biomarkers are incorporated into the pathophysiology of ARDS and lung problems. > This paper [26] briefly discusses the approach that though there are many clinical benefits specifying the importance to produce treatment for sparse diseases and cancer but the impact on the dealing and control of quite composite diseases, like type 2 diabetes, remains too low. This paper primarily specifies the ways by which people fall as a prey to poor health through the appliance of diagnostic labels. This review suggests a different, 'palette' model, center placed on a molecular taxonomy that aims on positioning an individual in accordance to the most pathophysiological processes that put-up to the risk and development of diabetes.

[15] Longitudinal multi-omic signatures of ARDS and sepsis inflammatory phenotypes identify key pathways associated with mortality

  • Authors: N. Alipanah-Lechner, L. Neyton, Pratik Sinha, Carolyn Leroux, K. Bardillon et al.
  • Year: 2025
  • Venue: medRxiv
  • URL: https://www.semanticscholar.org/paper/7ac6ad9892581d7caf0f6dd0c6c799180f575391
  • DOI: 10.1101/2025.05.07.25327117
  • PMID: 40963763
  • PMCID: 12440049
  • Citations: 3
  • Summary: Analysis of blood samples from ARDS patients in the ROSE trial revealed metabolomic and transcriptomic differences between Hyperinflammatory and Hypoinflammatory phenotypes and suggest potential therapeutic targets for precise treatment strategies in critical illness.
  • Evidence snippets:
  • Snippet 1 (score: 0.432) > The acute respiratory distress syndrome (ARDS) and sepsis are devastating critical illness syndromes with unacceptably high mortality rates approaching 40-50% in the United States (1,2). A significant challenge to developing effective treatments has been the marked heterogeneity in clinical presentation, underlying biology, and treatment responses among affected patients (3,4). > Recent advances in molecular phenotyping have identified reproducible subgroups of ARDS and sepsis patients with distinct pathobiology. Latent class analyses (LCA) of clinical and plasma protein data consistently reveal two predominant phenotypes: a "Hyperinflammatory" phenotype characterized by elevated plasma inflammatory protein biomarkers, shock, and higher mortality, and a "Hypoinflammatory" phenotype with relatively lower inflammatory protein biomarkers and better outcomes (5)(6)(7)(8)(9)(10). These phenotypes, identified across multiple ARDS and sepsis cohorts, demonstrate differential therapeutic responses in secondary analyses of randomized trials, suggesting they represent endotypes with distinct disease mechanisms (5,11,12). Clinical trials incorporating prospective phenotyping are being developed, including the PANTHER trial, which will start enrolling in mid-2025 (13). However, the biological processes driving each phenotype and mechanisms underlying unfavorable outcomes within each phenotype remain poorly understood. While protein biomarker studies have provided valuable insights into inflammatory patterns, they capture only a small fraction of the complex molecular landscape. > Previous metabolic profiling of 93 patients with ARDS demonstrated that the Hyperinflammatory phenotype exhibits reduced circulating lipids and a glycolytic shift, while transcriptomic analyses revealed increased expression of genes related to the innate immune response and tissue remodeling and reduced interferon signaling (10,14). However, isolatedomic approaches may miss critical interactions between cellular programming and systemic metabolism essential for understanding disease processes and treatment responses. > In this study, we applied longitudinal multi-omics profiling to characterize the molecular basis of ARDS/sepsis inflammatory phenotypes and identify mechanisms associated with poor outcomes.

[16] Development and functional significance of the pulmonary surfactant system

  • Authors: R. Shakhbanov, M. N. Asadulaeva, S.N. Alieva, A.A. Alimkhanova
  • Year: 2021
  • Venue: RUDN Journal of Medicine
  • URL: https://www.semanticscholar.org/paper/659ee76d2589b60002a27426d73bbf9734de6c63
  • DOI: 10.22363/2313-0245-2021-25-4-321-331
  • Citations: 2
  • Summary: To increase the effectiveness of pharmacological and respiratory therapy of acute respiratory distress syndrome, as well as to identify the role of the surfactant system of the lungs in the onset of inflammation against the background of tuberculosis and the development of regeneration mechanisms that affect the course and outcome of the disease.
  • Evidence snippets:
  • Snippet 1 (score: 0.429) > Relevance. Prevention of the development of postoperative acute respiratory distress syndrome during operations on the descending thoracic aorta increases the effectiveness of therapy. The study of damage to the surfactant complex during ischemia and reperfusion of the lungs is relevant, since it involves the prophylactic use of the surfactant preparation during operations on the descending part of the thoracic aorta, which are characterized by a high risk of postoperative acute respiratory distress syndrome. Objective: to increase the effectiveness of pharmacological and respiratory therapy of acute respiratory distress syndrome, as well as to identify the role of the surfactant system of the lungs in the onset of inflammation against the background of tuberculosis and the development of regeneration mechanisms that affect the course and outcome of the disease. Materials and Methods. The study involved 24 people, including 14 volunteer patients with a diagnosed respiratory disease in an acute course (while the whole group received the drug from the study as an additional therapy). The sample of 14 people was formed solely due to the compliance of these patients with the criteria that were established before the start of the study of the drug, which had postoperative acute respiratory distress syndrome of various origins in their diagnosis. Results and Discussion. For a comprehensive laboratory determination, an algorithm was used that corresponded to the state standard to identify postoperative acute respiratory distress syndrome. For each participant in the experiments, it was proposed to develop a plan of treatment procedures, taking into account individualization and standardization. Conclusion. Some of the resulting data are collected with respect to the surfactant pulmonary system, which is presented in a compactor model format. A number of basic components are reflected here, which are classified according to cellular and non-cellular factors. At the same time, the surfactant substance helps to reduce the pronounced swelling, which can significantly reduce the process of sticking of the alveolar structures during inhalation. All this added up to the normal system of gas metabolism in the lung structures, including the control of the mucociliary system, which acts as a natural stimulator of the function of alveolar macrophages.

[17] Values of integration between lipidomics and clinical phenomes in patients with acute lung infection, pulmonary embolism, or acute exacerbation of chronic pulmonary diseases: a preliminary study

  • Authors: Danyan Gao, Linlin Zhang, Dongli Song, Jiapei Lv, Linyan Wang et al.
  • Year: 2019
  • Venue: Journal of Translational Medicine
  • URL: https://www.semanticscholar.org/paper/bfd5c241ee1900a466476b56326304c9c9e0d73a
  • DOI: 10.1186/s12967-019-1898-z
  • PMID: 31109325
  • PMCID: 6528323
  • Citations: 22
  • Summary: It is demonstrated that lipidomic profiles of patients with acute lung diseases are different from healthy lungs, and there are also disease-specific portions of lipidomics among SAP, APE, or AECOPD.
  • Evidence snippets:
  • Snippet 1 (score: 0.428) > Acute lung injury is a major challenge and cause of patient morbidity and mortality in pulmonary critical care units, as an early stage of acute respiratory distress syndrome (ARDS), although molecular diagnosis and therapy are still lacking due to the complex pathogenesis, severity, and systemic responses [1]. Acute infection is one of common factors that can induce the exacerbation of chronic lung diseases. Chen et al., initially identified disease-specific dynamic biomarkers for severe pneumonia or severe pneumonia-associated-ARDS by integrating proteomic profiles of inflammatory mediators with clinical informatics as part of clinical bioinformatics [2]. They found that specific protein-based biomarkers comparing diseased tissue with healthy tissue and diseased tissue and diseased tissue had a significant correlation with clinical phenomes measured by Digital Evaluation Score System (DESS) scores. Shi et al. identified specific immunomodulatory mediators by evaluating dynamic genomic and proteomic profiles of peripheral blood mononuclear cells and plasma in patients with acute exacerbation of chronic obstructive pulmonary disease (AECOPD) and found a complex network of AECOPD-or COPD-specific immunomodulatory mediators [3]. In addition to changes of genomic and proteomic profiles, alterations of systemic metabolisms are also another important factor which can influence disease severity, duration, progression, and patient response to therapy, although the metabolism has been ignored in understanding of molecular mechanisms in the development of acute and chronic pulmonary diseases. > Clinical lipidomics is a new integrative approach to identify the disease-specific correlation and regulation between a large scale of lipid elements measured in liquid biopsies from patients with their clinical phenomes [4]. Clinical lipidomics has been suggested as a novel approach in discovering new categories of disease-specific biomarkers or therapeutic targets and could play a key role in improving our understanding of molecular mechanisms in disease metabolisms [5]. However, challenges still remain to be faced and overcome in prior to clinical practice [6].

[18] Enhanced mortality prediction in pneumonia-associated acute respiratory distress syndrome: a model integrating lymphocyte subsets with clinical parameters in non-immunosuppressed adults

  • Authors: Z. Xing, Hua Guo, Ting Ao, Jin-Xiang Wang, Ming Hu
  • Year: 2026
  • Venue: Frontiers in Medicine
  • URL: https://www.semanticscholar.org/paper/c51c13a1a85020abf45c9c16509242a87294f662
  • DOI: 10.3389/fmed.2026.1844614
  • PMID: 42245930
  • PMCID: 13230041
  • Summary: A multidimensional model for predicting in-hospital mortality in non-immunosuppressed adult patients with pneumonia-associated ARDS was developed and demonstrated excellent predictive performance, which was significantly higher than that of the baseline model.
  • Evidence snippets:
  • Snippet 1 (score: 0.426) > Acute respiratory distress syndrome (ARDS) is a critical clinical syndrome characterized by diffuse pulmonary inflammation and damage to the alveolar epithelial-capillary barrier. The clinical, physiological, biological and imaging manifestations of ARDS are highly heterogeneous. It is primarily be divided into two types: intrapulmonary and extrapulmonary. The condition manifests as progressive respiratory distress and refractory hypoxemia (1)(2)(3). Despite substantial advancements in mechanical ventilation strategies and supportive care in recent years, ARDS continues to be a relatively frequent condition associated with high morbidity and mortality, with severe ARDS cases exhibiting mortality rates as high as 46-66% (4-7). Pneumonia constitutes a major etiological factor for ARDS, accounting for approximately 59% of all ARDS cases (5). In patients with pneumoniaassociated acute respiratory distress syndrome (p-ARDS), the interplay between the initial pathogen invasion and the dysregulated host immune response serves as a critical determinant of clinical progression and prognosis. > The Sequential Organ Failure Assessment (SOFA) score and the CURB-65 score are clinically established tools for quantifying the extent of organ dysfunction and predicting mortality in pneumonia patients. These tools primarily serve to assess the extent of physiological dysfunction but demonstrate significant limitations in evaluating underlying pathophysiological mechanisms, particularly the immune status. In studies of COVID-19-related ARDS, immune dysregulation has been identified as a core feature of the disease pathophysiology, typically manifesting as significant lymphopenia and alterations in the distribution and function of key lymphocyte subsets, such as helper T cells (8). Meanwhile, pertinent studies have confirmed that adaptive immune impairment occurs during sepsis. The increased apoptosis of T cells, B cells, and dendritic cells drives a shift in the immune system from an initial pro-inflammatory state toward an anti-inflammatory and immunosuppressive response, potentially resulting in immunosuppression (9).

[19] [Genetic predisposition and Pediatric Acute Respiratory Distress Syndrome: New tools for genetic study].

  • Authors: B. Erranz, Jan Wilhelm, Raquel Riquelme, Pablo Cruces
  • Year: 2015
  • Venue: Revista chilena de pediatria
  • URL: https://www.semanticscholar.org/paper/9a0026c01cee098398beff7678483ecb888e06ce
  • DOI: 10.1016/j.rchipe.2015.04.016
  • PMID: 26235685
  • Summary: Genome-wide association studies can objectively examine variations of genes involved in key processes of tissue, cellular and molecular lung damage to help identify important new genes and pathogenetic pathways for future analysis and have diagnostic and therapeutic implications.
  • Evidence snippets:
  • Snippet 1 (score: 0.425) > Acute respiratory distress syndrome (ARDS) is the most severe form of respiratory failure. Theoretically, any acute lung condition can lead to ARDS, but only a small percentage of individuals actually develop the disease. On this basis, genetic factors have been implicated in the risk of developing ARDS. Based on the pathophysiology of this disease, many candidate genes have been evaluated as potential modifiers in patient, as well as in animal models, of ARDS. Recent experimental data and clinical studies suggest that variations of genes involved in key processes of tissue, cellular and molecular lung damage may influence susceptibility and prognosis of ARDS. However, the pathogenesis of pediatric ARDS is complex, and therefore, it can be expected that many genes might contribute. Genetic variations such as single nucleotide polymorphisms and copy-number variations are likely associated with susceptibility to ARDS in children with primary lung injury. Genome-wide association (GWA) studies can objectively examine these variations, and help identify important new genes and pathogenetic pathways for future analysis. This approach might also have diagnostic and therapeutic implications, such as predicting patient risk or developing a personalized therapeutic approach to this serious syndrome.

[20] Comorbidity Networks in Cardiovascular Diseases

  • Authors: Héctor A. Cruz-Ávila, M. Vallejo, M. Martínez-García, E. Hernández-Lemus
  • Year: 2020
  • Venue: Frontiers in Physiology
  • URL: https://www.semanticscholar.org/paper/1454c6cc3ca61441b24fd8c65ce02935b2845274
  • DOI: 10.3389/fphys.2020.01009
  • PMID: 32982776
  • PMCID: 7485389
  • Citations: 35
  • Influential citations: 1
  • Summary: It is found that comorbidity networks are highly centralized in prevalent diseases, such as cardiac arrhythmias, heart failure, chronic kidney disease, hypertension, and ischemic diseases, which may lead to further development of better, integrated therapeutic strategies.
  • Evidence snippets:
  • Snippet 1 (score: 0.424) > The first one of such pairs is formed by Other and unspecified encephalopathy (G93.4) and Acute respiratory distress syndrome (J80.X) with 437 common genes (JI = 0.827651515). These apparently disparate diseases share physiological and clinical associations. Burad et al. (2012) found that acute respiratory syndrome in pneumonia patients leads to strong systemic ischemia that may in turn develop into acute encephalopathy. This finding has been further confirmed in a very large (5.6 million cases) epidemiological risk factor study of the group of Bell in the US (Rincon et al., 2014). Aside from environmental and other risk factors, these diseases large number of shared genes are involved in a number of relevant biomolecular pathways, ranging from essential metabolism (folate-mediated one-carbon metabolism, antifolate resistance), signal transduction (cell adhesion, transendothelial leukocyte migration, a tight junction regulation). Also, including immune response and inflammation (response to hepatitis C, natural killer cell-mediated cytotoxicity, response to measles, Alzheimer's disease, and response to Influenza), as it was evidenced by gene enrichment analysis whose statistical significance was assessed via hypergeometric tests with false discovery rate multiple-testing correction (see Methods). > Closely related to this pair is the second one formed by Other and unspecified encephalopathy (G93.4) and Acute respiratory failure (J96.0) with 440 common genes representing a JI = 0.787119857, these genes refer to similar pathways involved with the addition of statistical enrichment of the protein digestion and absorption pathway. Understanding the role that such molecular processes may have in the onset and progression of both diseases, of the comorbidity and of their potential multimorbidity relations in the context of the CVCnetwork (see Figure 4), may prove useful, particularly in the design of combined therapeutic strategies with special emphasis in the critically ill patients in intensive care units. > In this regard, we may mention the following: it is known that the physiological manifestation of such biomolecular process starts in the microvascular endothelium (MVE).

Notes

  • This provider combines search_papers_by_relevance with snippet_search.
  • No synthesis or second-stage model call is performed.