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Thallium Poisoning

Asta Literature Retrieval: Disease Pathophysiology Research Template Target Disease Disease Name: Thallium Poisoning MONDO ID: (if available) Ca...

2026-03-17
Asta MONDO:0041996 Model: Asta Scientific Corpus Retrieval 19 citations

Asta Literature Retrieval: Disease Pathophysiology Research Template Target Disease Disease Name: Thallium Poisoning MONDO ID: (if available) Ca...

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

  • Papers retrieved: 19
  • Snippets retrieved: 20

Relevant Papers

[1] D-Penicillamine Reveals the Amelioration of Seizure-Induced Neuronal Injury via Inhibiting Aqp11-Dependent Ferroptosis

  • Authors: Nan Yang, Kai Zhang, Qiwen Guan, Zhaoxin Wang, Kang-Ni Chen et al.
  • Year: 2022
  • Venue: Antioxidants
  • URL: https://www.semanticscholar.org/paper/9cbcd9c66c77d092ea31947f5258f8e2a8185b0a
  • DOI: 10.3390/antiox11081602
  • PMID: 36009321
  • PMCID: 9405105
  • Citations: 19
  • Summary: DPA can be repurposed to cure seizure disorders such as epilepsy, and the effects of DPA on ferroptosis process are dependent upon Aqp11, a gene coding previously reported channel protein responsible for transporting water and small solutes.
  • Evidence snippets:
  • Snippet 1 (score: 0.516) > The present work focused on the effects of DPA on seizure-induced neuronal injury and its potential molecular mechanism. The major findings of the study are shown as follows: > (1) DPA exerts the pronounced protection against seizure-induced neuronal impairment; > (2) ferroptosis is involved in the amelioration of DPA on the injured neurons post seizure; > (3) Aqp11 is identified to be a key molecular target for the inhibitory effect of DPA on neuronal ferroptosis in vitro and on seizure-induced neuronal damage in vivo (Figure 7). DPA is a first-line drug for treating Wilson's disease in clinical practice, and, also, has wide therapeutic applications in curing chronic active hepatitis, rheumatoid arthritis, systemic sclerosis, primary biliary cirrhosis and so on [41][42][43][44][45]. Previously, DPA has been demonstrated to mitigate the neurotoxicity caused by heavy metal thallium [46]. It has been reported that thallium poisoning can lead to neurological abnormalities that affect lower limb motor function [46,47]. Combinational treatment with DPA and Prussian blue significantly prevents the dysfunction of purkinje cells in the brain of thallium poisoned rats. These data indicate the alleviation of neurotoxicity after DPA treatment. In addition, DPA is a first-line drug for treating Wilson's disease in clinical practice, and, also, has wide therapeutic applications in curing chronic active hepatitis, rheumatoid arthritis, systemic sclerosis, primary biliary cirrhosis and so on [41][42][43][44][45]. Previously, DPA has been demonstrated to mitigate the neurotoxicity caused by heavy metal thallium [46]. It has been reported that thallium poisoning can lead to neurological abnormalities that affect lower limb motor function [46,47]. Combinational treatment with DPA and Prussian blue significantly prevents the dysfunction of purkinje cells in the brain of thallium poisoned rats. These data indicate the alleviation of neurotoxicity after DPA treatment.

[2] Comprehensive review on the pathogenesis of hypertriglyceridaemia-associated acute pancreatitis

  • Authors: Minhao Qiu, Xiaoying Zhou, M. Zippi, Hemant Goyal, Zarrin Basharat et al.
  • Year: 2023
  • Venue: Annals of Medicine
  • URL: https://www.semanticscholar.org/paper/45eb6adcd7600f6a642f6adcf51182e2de45ba30
  • DOI: 10.1080/07853890.2023.2265939
  • PMID: 37813108
  • PMCID: 10563627
  • Citations: 44
  • Influential citations: 1
  • Summary: An overview of triglyceride metabolism and the potential mechanisms that may contribute to developing or exacerbating hypertriglyceridaemia appears promising, with ongoing research focused on developing more specific and effective treatment strategies.
  • Evidence snippets:
  • Snippet 1 (score: 0.514) > HTAP is a complex disease with a multifactorial aetiology, and not fully understood pathophysiology.As our knowledge regarding the disease evolves, we are likely to develop more effective and targeted treatments, which can reduce the occurrence of more severe disease outcomes or prevent the disease altogether.Future research will need to focus on elucidating the underlying genetic and molecular mechanisms of the disease, as well as identifying specific pathways and targets that can be used to develop more effective treatments.This will require a multidisciplinary approach that combines genetics, molecular biology, and clinical research and will likely involve collaborations between basic and clinical scientists across multiple disciplines.Ultimately, developing more effective treatments for HTAP will require a deep understanding of the underlying pathophysiology of the disease, as well as the development of more targeted and personalized approaches to diagnosis and treatment.

[3] Emerging Trends in Pathophysiology: Insights from the 9th International Congress of the International Society for Pathophysiology (ISP 2023)

  • Authors: A. Kubyshkin, S. Bolevich, L. Churilov, V. Jakovljevic, E. Kovalenko et al.
  • Year: 2024
  • Venue: Pathophysiology
  • URL: https://www.semanticscholar.org/paper/3ab0c7d37d984c72ca8cba300cb8052c1326e61a
  • DOI: 10.3390/pathophysiology31010011
  • PMID: 38535621
  • PMCID: 10975917
  • Summary: The main trends and the most promising areas of research in current pathophysiology, including investigations of new pathogenic pathways, and the identification of cellular and molecular mechanisms, target molecules, genetic mechanisms, and new therapeutic strategies are described.
  • Evidence snippets:
  • Snippet 1 (score: 0.494) > This article provides a summary of the 9th International Congress of the International Society for Pathophysiology (ISP 2023) which took place in Belgrade, Serbia, from 4 to 6 July 2023. It describes the main trends and the most promising areas of research in current pathophysiology, including investigations of new pathogenic pathways, and the identification of cellular and molecular mechanisms, target molecules, genetic mechanisms, and new therapeutic strategies. The present article also highlights the research conducted by leading scientific teams and national pathophysiological societies from various countries that adds to our understanding of the pathogenesis of diseases and pathological processes.

[4] Of Mice and Men: Comparative Analysis of Neuro-Inflammatory Mechanisms in Human and Mouse Using Cause-and-Effect Models

  • Authors: A. Kodamullil, Anandhi Iyappan, Reagon Karki, S. Madan, E. Younesi et al.
  • Year: 2017
  • Venue: Journal of Alzheimer's Disease
  • URL: https://www.semanticscholar.org/paper/55820fd5fc6231bc4bf3c0330cb6cbfea9a4827c
  • DOI: 10.3233/JAD-170255
  • PMID: 28731442
  • PMCID: 5545904
  • Citations: 27
  • Summary: This paper investigates the failure of a neuroinflammation targeted drug in the late phases of clinical trials based on the comparative analyses between the two species and assesses to what extend a mouse can mimic the cellular and molecular interactions in humans at a mechanism level.
  • Evidence snippets:
  • Snippet 1 (score: 0.473) > Mouse models are extensively used in biomedical research mainly to understand the etiology of the disease. Complex diseases like AD may involve several simultaneous alterations in molecular and processual activities, including neuroinflammation, aggregation of A␤ peptides, or tau phosphorylation, which are likely to contribute to pathophysiology. In this paper, we have compared the mouse and human at molecular, cellular, and pathway levels to shed light on mechanistic differences with important implications for translation outcomes. Mechanistic modelling specific to species allows us to "embed" and "represent" similarities and differences in innate immunity which can lead to the development of "conflictious information detection engine". It is important to note that our analysis is purely based on the research and publication bias in mouse and human experiments as many mouse experiments are mainly focused on particular explorative areas, and experiments with human tissues are also concentrated on limited areas of disease mechanism. We found that mouse experiments often reveal new molecular interactions between different entities that are not observed or reported in human experiments. Differential analysis of mouse and human model for neuroinflammation shows that mouse and human differ at the molecular and cellular levels, but have more similarities at the pathway levels as numbers indicate. More explicitly, the underlying molecular patterns which lead to a particular bioprocess differ between the two species. This finding implies that although the two species share some similarities at the cellular or pathway level, the pattern of molecular interactions that form, govern, and regulate those pathways is substantially different between mouse and human. > It is notable that mouse models have provided significant insights into many disease areas like cancer; acute promyelocytic leukemia. However, recent drug failures in the area of neurodegeneration have put a question mark behind the extent to which mouse models have been used in preclinical drug discovery and to what extent transgenic mice mimic human brain pathophysiology mechanisms. Pathophysiology mechanisms are likely to act together and they seem to be organized in a temporal cascade of events that ultimately result in a severe disease phenotype. Experiments with single gene knock-out in mice can reveal only minor aspects of the disease perturbations and do not usually allow us to decipher the full complexity of the mechanisms underlying the disease.

[5] Integrative human and murine multi-omics: Highlighting shared biomarkers in the neuronal ceroid lipofuscinoses.

  • Authors: N. Gammaldi, F. Pezzini, E. Michelucci, N. Di Giorgi, A. Simonati et al.
  • Year: 2023
  • Venue: Neurobiology of disease
  • URL: https://www.semanticscholar.org/paper/2c50113653b538549410afe59f69ce70a4184a43
  • DOI: 10.1016/j.nbd.2023.106349
  • PMID: 37952681
  • Citations: 3
  • Summary: The results offer promising targets for potential new therapeutic strategies and reinforce the hypothesis of a connection between NCLs and other forms of dementia, particularly Alzheimer's disease.
  • Evidence snippets:
  • Snippet 1 (score: 0.472) > Recent methodological advances in multi-omics approaches have revolutionized research in rare diseases by balancing the low availability of samples and the poor information about pathophysiology with the generation of "big data", which has greatly enhanced our understanding of the molecular complexity underlying these diseases. Omics data can be integrated correlating them from different sources and technologies in order to identify affected disease pathways, biomarkers, as well as new pharmaceutical targets. > In the brain, common dysregulated pathways have been identified not only in NCLs, but also in almost every late-onset neurodegenerative and aging-related disorder, suggesting that targeting these common pathways may open up promising new therapeutic opportunities (Kline et al., 2020;Kodam et al., 2023;Schilder et al., 2022). > In this review, we explored the pathogenesis of NCL disease, evaluating human data in order to define common molecular networks underlying the top dysregulated processes. Moreover, by distinguishing between pre-symptomatic and symptomatic stages, we were able to evaluate disease progression in murine models from both a cell-specific and an anatomical point of view. We evaluated the cellular microenvironment, highlighting the main altered pathways and pinpointing processes implicated across species and in single forms. The results generated pave the way for identifying the different brain regions primarily affected by the disease.
  • Snippet 2 (score: 0.441) > Poor information on disease pathophysiology, and therefore on possible disease biomarkers, is a major obstacle to clinical trials in this field. Exploration of disease pathways likely shared by NCLs, such as oxidative phosphorylation, mitochondrial bioenergetics, autophagy (either macro-or mitophagy), and lysosomal clearance, may facilitate the process of biomarker discovery, making it possible to identify novel targets useful for monitoring disease status and progression, and accelerating trial readiness in patients. > The research field has recently benefited from the development of omics approaches allowing the generation of huge amounts of information even from small numbers of biological samples or cases. > Transcriptomics, in particular, has advanced considerably in recent years. Microarray platforms and high-throughput RNA sequencing have allowed high coverage of the human transcriptome, as well as that of the main animal models of the disease. > Proteomics, on the other hand, involving the use of mass spectrometry-based technologies, provides the most accurate insight into cellular physiology and disease biomarkers. Furthermore, new emerging disciplines are allowing the assessment of metabolomic and lipidomic analyses, increasing available information on the interplay between genes and the environment. > In this setting, one of the major challenges when seeking to determine the mechanisms underlying biological processes is sample complexity, given the possible presence of splice variants and/or posttranslational modification (Al-Amrani et al., 2021); another is the large volume of generated data, which require a validation process using different, non-omics approaches. > Although human samples, such as biological fluids, patient fibroblasts, and post-mortem tissues are, traditionally, the main samples used to investigate genetic, clinical, and biochemical factors, the increasing availability of in vitro and in vivo disease models has facilitated our understanding of disease pathophysiology and the screening of possible therapeutic targets.

[6] Novel Insights into the Molecular Mechanisms of Atherosclerosis

  • Authors: Armanda Wojtasińska, W. Frąk, Wiktoria Lisińska, Natalia Sapeda, Ewelina Młynarska et al.
  • Year: 2023
  • Venue: International Journal of Molecular Sciences
  • URL: https://www.semanticscholar.org/paper/fae6fbd9d1854df6a8d53eb43525ea8ec5af1cd7
  • DOI: 10.3390/ijms241713434
  • PMID: 37686238
  • PMCID: 10487483
  • Citations: 50
  • Summary: This review summarizes the available information on the pathophysiological implications of atherosclerosis, focusing on endothelium dysfunction, inflammatory factors, aging, and uric acid, vitamin D, and miRNA expression as recent evidence of interactions of the molecular and cellular elements.
  • Evidence snippets:
  • Snippet 1 (score: 0.471) > Atherosclerosis is one of the most fatal diseases in the world. The associated thickening of the arterial wall and its background and consequences make it a very composite disease entity with many mechanisms that lead to its creation. It is an active process, and scientists from various branches are engaged in research, including molecular biologists, cardiologists, and immunologists. This review summarizes the available information on the pathophysiological implications of atherosclerosis, focusing on endothelium dysfunction, inflammatory factors, aging, and uric acid, vitamin D, and miRNA expression as recent evidence of interactions of the molecular and cellular elements. Analyzing new discoveries for the underlying causes of this condition assists the general research to improve understanding of the mechanism of pathophysiology and thus prevention of cardiovascular diseases.

[7] Pathogenesis and Therapeutic Perspectives of Tubular Injury in Diabetic Kidney Disease: An Update

  • Authors: Jiamian Geng, Sijia Ma, Hui Tang, Chun-di Zhang
  • Year: 2025
  • Venue: Biomedicines
  • URL: https://www.semanticscholar.org/paper/889b3498a05a86b303b0fc3bd0f89915c65f39f0
  • DOI: 10.3390/biomedicines13061424
  • PMID: 40564143
  • PMCID: 12189843
  • Citations: 3
  • Summary: Advances in stem cell-based interventions and precision gene editing techniques have unveiled novel therapeutic paradigms for DKD, fundamentally expanding the treatment arsenal beyond conventional pharmacotherapy and highlighting promising therapeutic strategies for managing this condition.
  • Evidence snippets:
  • Snippet 1 (score: 0.468) > The adaptive mechanisms of cellular stress responses play a pivotal role in maintaining organismal homeostasis, conferring remarkable resilience against pathological processes and disease progression [65]. In the context of DKD, three primary forms of stress response mechanisms have been implicated in disease pathogenesis and clinical progression. These maladaptive responses manifest as oxidative stress-mediated cellular damage, ERS-induced protein homeostasis disruption, and mitochondrial dysfunction-related metabolic disturbances. Each pathway contributes distinctively to the complex pathophysiology of DKD through interconnected mechanisms of cellular injury and aberrant signaling cascades.

[8] Lactate metabolism and lactylation in kidney diseases: insights into mechanisms and therapeutic opportunities

  • Authors: Yuhua Cheng, Linjuan Guo
  • Year: 2025
  • Venue: Renal Failure
  • URL: https://www.semanticscholar.org/paper/6208b88884af543f7c97d2e70ed6b727dcfb4f58
  • DOI: 10.1080/0886022X.2025.2469746
  • PMID: 40012230
  • PMCID: 11869332
  • Citations: 9
  • Summary: A review examines the role of lactate esters, especially lactylation, in kidney diseases, with a focus on their regulatory mechanisms and potential as therapeutic targets.
  • Evidence snippets:
  • Snippet 1 (score: 0.463) > Lactate metabolism and its post-translational modifications, particularly lactylation, play critical roles in the pathophysiology of various kidney diseases, including AKI, DKD, and ccRCC (Figure 1). The kidney's ability to metabolize lactate is crucial for maintaining renal function under normal conditions. However, in pathological states, impaired lactate metabolism leads to its accumulation, exacerbating renal dysfunction and disease progression. For more details on lactate metabolism and kidney diseases, refer to previous reviews [2,3,25]. > Lactylation influences gene transcription, protein function, and cellular metabolism, contributing to inflammatory responses, mitochondrial dysfunction, and tumor progression. > Understanding the mechanisms of lactate metabolism and lactylation in kidney diseases opens new avenues for therapeutic interventions. Targeting these metabolic pathways could mitigate renal injury and improve patient outcomes. Future research should focus on elucidating the specific pathways and molecular targets affected by lactate and lactylation and developing inhibitors to modulate these processes. Clinical trials are necessary to validate the efficacy and safety of these therapies. Overall, the lactate-lactylation axis is a promising target for novel therapeutic strategies aimed at treating kidney diseases and improving renal health.

[9] Lessons from Toxicology: Developing a 21st-Century Paradigm for Medical Research

  • Authors: G. Langley, C. Austin, A. Balapure, L. Birnbaum, J. Bucher et al.
  • Year: 2015
  • Venue: Environmental Health Perspectives
  • URL: https://www.semanticscholar.org/paper/b54081862ef66a83e34fe6a9c2586bc58b459c28
  • DOI: 10.1289/ehp.1510345
  • PMID: 26523530
  • PMCID: 4629751
  • Citations: 59
  • Summary: A new conceptual framework that repurposes the 21st-century transition underway in toxicology is suggested, conceived as resulting from integrated extrinsic and intrinsic causes, with research focused on modern human-specific models to understand disease pathways at multiple biological levels.
  • Evidence snippets:
  • Snippet 1 (score: 0.455) > In the context of disease research and drug discovery, our disease AOP concept would provide a unified framework for describing relevant pathophysiological pathways and networks across multiple biological levels and for encompassing extrinsic and intrinsic causes. Describing these pathways and networks, along with anchoring molecular initiating events with adverse outcomes, our AOP frame work would represent a significant advance over existing concepts, such as disease mechanisms that are often studied in isolation and biological pathways or networks (e.g., for cancers) that are invariably considered only at the molecular or cellular levels. > The disease AOP approach would better exploit advanced experimental and computational platforms for knowledge discovery, since the emergence of AOP networks will identify knowledge gaps and steer investigations accordingly. A commitment to build, curate, and disseminate a pathways framework within the biomedical research field would thus provide considerable impetus to base decisions on mechanistic understanding rather than empirical observation, as has been the case in toxicology. > Advanced human-specific disease models. In addition to a stra tegic and integrated knowledgebased exploitation of omics tools and the introduction of the AOP concept, we further propose a strong focus on humanspecific models. Advanced humanspecific cell and tissuebased models (e.g., Singh et al. 2011) and nextgeneration tools are making possible a fuller, dynamic comprehension of disease pathophysiology and a more reliable and costeffective drug discovery process (Muotri 2015). > Humaninduced pluripotent stem cell technology offers unique access to healthy as well as patient and diseasespecific in vitro cell models (Bellin et al. 2012). This could help achieve the holy grail of Figure 1. Integrating data on extrinsic and intrinsic causes of disease using systems biology provides a more comprehensive understanding of human illnesses. The adverse outcome pathway (AOP) concept links exposure, via chemical structure (or structures), the molecular initiating event, and key events, to an adverse outcome.

[10] Neurodevelopmental models of transcription factor 4 deficiency converge on a common ion channel as a potential therapeutic target for Pitt Hopkins syndrome

  • Authors: Matthew D. Rannals, S. Page, Morganne N. Campbell, Ryan A. Gallo, Brent Mayfield et al.
  • Year: 2016
  • Venue: Rare Diseases
  • URL: https://www.semanticscholar.org/paper/5527675a93315291579d926c05b804d7c82e2090
  • DOI: 10.1080/21675511.2016.1220468
  • PMID: 28032012
  • PMCID: 5154382
  • Citations: 26
  • Influential citations: 2
  • Summary: It is demonstrated that haploinsufficiency of TCF4 lead to the ectopic expression of two ion channels, Scn10a and Kcnq1, which indicates SCN10a is a potential therapeutic target for Pitt-Hopkins syndrome.
  • Evidence snippets:
  • Snippet 1 (score: 0.448) > Determining the underlying mechanisms of pathophysiology for rare diseases, as well as for more common disorders, is a formidable challenge. Here, and in our recent article, 13 we have described a system for phenotype discovery in a rare disease model that utilizes a novel molecular profiling method we term iTRAP that is capable of identifying candidate molecular mechanisms underlying pathophysiological phenotypes. > By comparing a cell autonomous TCF4 haploinsufficiency rat model to a PTHS mouse model, we identified a common electrophysiological phenotype that is at least partially caused by inappropriate expression of Scn10a, a voltage-gated sodium channel. We now consider SCN10a to be a potential therapeutic target for PTHS. Further experiments are required to determine if these phenotypes and molecular mechanisms observed at the cellular level can be successfully translated to the level of mouse behavior, to human biology, and ultimately to the development of therapeutic agents.

[11] Changes in Serum Proteomic Profiles at Different Stages of Pregnancy Toxemia in Goats

  • Authors: M. Uzti̇mür, C. N. Ünal, Gurler Akpinar
  • Year: 2025
  • Venue: Journal of Veterinary Internal Medicine
  • URL: https://www.semanticscholar.org/paper/4b9c488b5dbd65d7b26fd2ad9aed70e8c4b59942
  • DOI: 10.1111/jvim.70139
  • PMID: 40492724
  • PMCID: 12150350
  • Summary: Understanding the serum proteome profiles of goats with pregnancy toxemia might help identify the proteomes and pathways responsible for the development of this disease and improve diagnosis and treatment.
  • Evidence snippets:
  • Snippet 1 (score: 0.444) > The pathophysiology and progression of this disease are not fully understood. > Traditional biomedical research has focused on the analysis of single genes, proteins, metabolites, or metabolic pathways in diseases. This molecular reductionist approach is based on the assumption that identifying genetic variations and molecular components will lead to new treatments for diseases [13][14][15][16]. However, many diseases are complex and multifactorial, and in order to determine the phenotype of such diseases, it is necessary to understand the changes that occur in more than one gene, pathway, protein, or metabolite at the cellular, tissue, and organismal levels [17][18][19]. Therefore, in recent years, proteomics, as one field of multi-omics technologies, has helped in evaluating the complex pathogenetic mechanisms of different diseases from a broad perspective and has made substantial contributions [20,21]. In veterinary medicine, proteomic analysis of metabolic diseases such as ketosis [16], hypocalcemia [22], and fatty liver [23] in dairy cows has contributed valuable insights for the definition of new pathophysiological pathways and new diagnosis and treatment protocols for these diseases. The proteomic approach can contribute importantly to a broad and detailed understanding of the changes that occur at the organismal level associated with the increase in BHBA concentration in goats with pregnancy toxemia. Our aim was to evaluate the serum protein profiles of goats with SPT or CPT using proteomic techniques to determine the proteomic profiles of these animals and to identify the relevant pathophysiological mechanisms.

[12] Signaling pathways involved in ischemic stroke: molecular mechanisms and therapeutic interventions

  • Authors: C. Qin, Sheng Yang, Yun-hui Chu, Hang Zhang, Xiaoyi Pang et al.
  • Year: 2022
  • Venue: Signal Transduction and Targeted Therapy
  • URL: https://www.semanticscholar.org/paper/c228d67d7d6468e6610bf3880e81d8510ed5a25b
  • DOI: 10.1038/s41392-022-01064-1
  • PMID: 35794095
  • PMCID: 9259607
  • Citations: 682
  • Influential citations: 17
  • Summary: This review elucidated potential molecular mechanisms and related signaling pathways underlying ischemic stroke, and summarize the therapeutic approaches targeted various pathophysiology, with particular reference to clinical trials and future prospects for treating isChemic stroke.
  • Evidence snippets:
  • Snippet 1 (score: 0.443) > Ischemic stroke is caused primarily by an interruption in cerebral blood flow, which induces severe neural injuries, and is one of the leading causes of death and disability worldwide. Thus, it is of great necessity to further detailly elucidate the mechanisms of ischemic stroke and find out new therapies against the disease. In recent years, efforts have been made to understand the pathophysiology of ischemic stroke, including cellular excitotoxicity, oxidative stress, cell death processes, and neuroinflammation. In the meantime, a plethora of signaling pathways, either detrimental or neuroprotective, are also highly involved in the forementioned pathophysiology. These pathways are closely intertwined and form a complex signaling network. Also, these signaling pathways reveal therapeutic potential, as targeting these signaling pathways could possibly serve as therapeutic approaches against ischemic stroke. In this review, we describe the signaling pathways involved in ischemic stroke and categorize them based on the pathophysiological processes they participate in. Therapeutic approaches targeting these signaling pathways, which are associated with the pathophysiology mentioned above, are also discussed. Meanwhile, clinical trials regarding ischemic stroke, which potentially target the pathophysiology and the signaling pathways involved, are summarized in details. Conclusively, this review elucidated potential molecular mechanisms and related signaling pathways underlying ischemic stroke, and summarize the therapeutic approaches targeted various pathophysiology, with particular reference to clinical trials and future prospects for treating ischemic stroke.

[13] The use of intra-cellular signaling pathways in anesthesiology and pain medicine field.

  • Authors: J. Joo
  • Year: 2009
  • Venue: Korean journal of anesthesiology
  • URL: https://www.semanticscholar.org/paper/d20f7ea110adebeb95be021611d90522a87a42c1
  • DOI: 10.4097/kjae.2009.57.3.277
  • PMID: 30625873
  • Citations: 1
  • Summary: If efforts are focused on applying the new cellular and molecular biologic research, these efforts could identify the mechanism of diseases and help develop new drugs in the field of anesthesiology and pain medicine.
  • Evidence snippets:
  • Snippet 1 (score: 0.442) > At the level of individual cells, signaling is crucial in cell division, differentiation, metabolic control and death. Reception of the signals depends on receptor proteins that are usually at the cell surface, and these receptor proteins bind the signal molecule. The binding activates the receptor, which in turn activates one or more of the intra-cellular signaling pathways. These relay chains of molecules, mainly intra-cellular signaling proteins, process the signal inside the receiving cell and distribute it to the appropriate intra-cellular targets. Cell signaling pathways are involved in the pathophysiology of many diseases and also in the mechanisms of action of many drugs, including local and general anesthetics. Knowledge of the basic cell signaling mechanisms is essential for understanding many of the pathophysiologic and pharmacologic mechanisms. Therefore, if we focus on applying the new cellular and molecular biologic research, these efforts could identify the mechanism of diseases and help develop new drugs in the field of anesthesiology and pain medicine.

[14] A framework for integrating evidence to assess hazards and risk

  • Authors: Sandra I Sulsky, Tracy Greene, P. Gentry
  • Year: 2024
  • Venue: Critical Reviews in Toxicology
  • URL: https://www.semanticscholar.org/paper/dbbeed8f2ab91451a96ae1d432e50cfb0277a371
  • DOI: 10.1080/10408444.2024.2342447
  • PMID: 38808643
  • Citations: 1
  • Summary: This novel evidence integration framework (EIF) provides a method for synthesizing data from comprehensive, systematic, quality-based assessments of the epidemiological and toxicological literature, including in vivo and in vitro mechanistic studies, providing a method to support evidence synthesis.
  • Evidence snippets:
  • Snippet 1 (score: 0.439) > Similarly, toxicological studies may be based on a hypothesis regarding relationships between exposures and outcomes without a solid evidence base.These factors complicate the synthesis of the data and can make it difficult to identify concordance between human health outcomes and the types of endpoints studied toxicologically.The value of the EIF is its inclusion of all available information, and its explicit discussion of sources of uncertainty and the effect of uncertainty on the conclusions that can be drawn. > The disease-based component of the EIF is driven by the diseases observed and evaluated in humans and is enhanced by an understanding of the pathophysiology of those specific diseases.It allows for consideration of endpoints that mark the progression of disease, if they are measurable in humans or animals, but it does not address potential initiating events or include assay results at the cellular level that are not linked to identifiable human pathology.In addition, endpoints that share common biological mechanisms, but not similar pathophysiological manifestations, are often considered relevant to different disease groupings.Therefore, applying the disease-based categorization system requires an additional integrative step to identify common modes of action across specific diseases within a group. > In contrast, the mechanism-based component of the EIF accounts for general mechanisms of disease causation and can incorporate assay results at the cellular level that have been used as potential indicators of disease risk (e.g.Ames assay).Poor or incomplete understanding of the mechanisms leading to diseases proposed to be associated with exposure will increase the level of uncertainty of the conclusions.Recognizing and delineating these uncertainties in basic medical and scientific knowledge may direct future research decisions. > As much as the EIF aims to be objective and to make explicit the processes for rating and weighting the available evidence, some qualitative, subjective elements remain.Professional judgment is required to rate the quality of the underlying studies and to determine which human and toxicological endpoints are related sufficiently to be grouped together.The disease-based approach to organizing the toxicological data relies on the original authors' definitions of outcomes and their study purposes, which influence the conclusions drawn from the evidence integration.

[15] Mitochondrial Dysfunction in Diabetes: Shedding Light on a Widespread Oversight

  • Authors: F. Iheagwam, A. J. Joseph, E. D. Adedoyin, Olawumi Toyin Iheagwam, Samuel Akpoyowvare Ejoh
  • Year: 2025
  • Venue: Pathophysiology
  • URL: https://www.semanticscholar.org/paper/dbf8042761c1a5fc50f8cd894cc498505abac7cb
  • DOI: 10.3390/pathophysiology32010009
  • PMID: 39982365
  • PMCID: 12077258
  • Citations: 22
  • Summary: This review aims to elucidate the complex link between mitochondrial dysfunction and diabetes, covering the spectrum of diabetes types, the role of mitochondria in insulin resistance, highlighting pathophysiological mechanisms, mitochondrial DNA damage, and altered mitochondrial biogenesis and dynamics.
  • Evidence snippets:
  • Snippet 1 (score: 0.438) > The landscape of DM research is continuously evolving, with emerging technologies and approaches offering new insights into the pathophysiology of the disease and potential therapeutic targets. Advancements in omics technologies, encompassing genomes, transcriptomics, proteomics, and metabolomics, have transformed the molecular mechanisms underlying DM [134]. High-throughput sequencing techniques enable comprehensive analysis of genetic variants, gene expression profiles, protein abundance, and metabolite levels associated with DM and its complications [135]. Single-cell omics approaches provide unprecedented resolution and granularity, allowing researchers to dissect cellular heterogeneity and identify novel cell types, subpopulations, and signalling pathways involved in DM pathogenesis. Integrating multi-omics data sets offers a systems-level perspective of DM, unravelling complex networks of molecular interactions and regulatory circuits underlying disease progression [136]. > In addition to omics technologies, advances in imaging modalities, such as MRI, PET, and optical imaging, enable non-invasive visualisation and quantification of metabolic, functional, and structural changes. Molecular imaging probes targeting specific biomarkers and metabolic pathways provide valuable insights into disease mechanisms and treatment responses in preclinical and clinical settings [85]. Despite significant progress in DM research, numerous unanswered questions and knowledge gaps persist, hindering the ability to develop effective prevention and treatment strategies. Key areas requiring further investigation include the role of epigenetics, environmental factors, and the microbiome in DM susceptibility and progression. Moreover, the interaction between environmental cues and genetic predisposition remains incompletely understood, highlighting the need for comprehensive multi-omics studies and large-scale epidemiological analyses to identify gene-environment interactions and modifiable risk factors for DM [137]. Furthermore, the heterogeneity of DM phenotypes and clinical outcomes poses a challenge for personalised medicine approaches, necessitating robust biomarkers and predictive models to stratify patients based on disease subtypes, prognosis, and treatment response [138].

[16] Extracellular Cold-Inducible RNA-Binding Protein: Progress from Discovery to Present

  • Authors: M. Aziz, I. Chaudry, Ping Wang
  • Year: 2025
  • Venue: International Journal of Molecular Sciences
  • URL: https://www.semanticscholar.org/paper/c47336a8ca38d2a39d9f4ae2bc3a3bfd47063ccb
  • DOI: 10.3390/ijms26083524
  • PMID: 40332009
  • PMCID: 12026706
  • Citations: 3
  • Summary: The molecular, cellular, and immunological mechanisms through which eCIRP contributes to disease progression, and the potential therapeutic strategies targeting eCIRP in preclinical models of inflammatory and ischemic diseases are explored.
  • Evidence snippets:
  • Snippet 1 (score: 0.438) > Extracellular cold-inducible RNA-binding protein (eCIRP) is a critical damage-associated molecular pattern (DAMP) that drives inflammation and tissue injury in hemorrhagic and septic shock, and has emerged as a promising therapeutic target. Since then, extensive research using preclinical models of diseases and patient materials has explored eCIRP’s role in driving inflammatory responses and its potential as a biomarker. The main objective of this comprehensive review is to provide a detailed overview of eCIRP, covering its discovery, role in disease pathophysiology, mechanisms of release and action, potential as a biomarker, and therapeutic strategies targeting eCIRP in preclinical models of inflammatory and ischemic diseases. We examine the molecular, cellular, and immunological mechanisms through which eCIRP contributes to disease progression, and explore both well-established and emerging areas of research. Furthermore, we discuss potential therapeutic strategies targeting eCIRP across a broad spectrum of inflammatory conditions, including shock, ischemia–reperfusion injury, neurodegenerative diseases, and radiation injury.

[17] Signaling pathways and potential therapeutic targets in acute respiratory distress syndrome (ARDS)

  • Authors: Qian-rui Huang, Yue Le, Shusheng Li, Yi Bian
  • Year: 2024
  • Venue: Respiratory Research
  • URL: https://www.semanticscholar.org/paper/886cb171076bcc2ba770b87ab0fae9baa96120ba
  • DOI: 10.1186/s12931-024-02678-5
  • PMID: 38218783
  • PMCID: 10788036
  • Citations: 57
  • Influential citations: 1
  • Summary: The pathogenesis and pathophysiology of ARDS that involve dysregulated inflammation, alveolar-capillary barrier dysfunction, impaired alveolar fluid clearance and oxidative stress are described and the emerging therapeutic strategies that show exciting promise are discussed.
  • Evidence snippets:
  • Snippet 1 (score: 0.437) > Acute respiratory distress syndrome (ARDS) is a common condition associated with critically ill patients, characterized by bilateral chest radiographical opacities with refractory hypoxemia due to noncardiogenic pulmonary edema. Despite significant advances, the mortality of ARDS remains unacceptably high, and there are still no effective targeted pharmacotherapeutic agents. With the outbreak of coronavirus disease 19 worldwide, the mortality of ARDS has increased correspondingly. Comprehending the pathophysiology and the underlying molecular mechanisms of ARDS may thus be essential to developing effective therapeutic strategies and reducing mortality. To facilitate further understanding of its pathogenesis and exploring novel therapeutics, this review provides comprehensive information of ARDS from pathophysiology to molecular mechanisms and presents targeted therapeutics. We first describe the pathogenesis and pathophysiology of ARDS that involve dysregulated inflammation, alveolar-capillary barrier dysfunction, impaired alveolar fluid clearance and oxidative stress. Next, we summarize the molecular mechanisms and signaling pathways related to the above four aspects of ARDS pathophysiology, along with the latest research progress. Finally, we discuss the emerging therapeutic strategies that show exciting promise in ARDS, including several pharmacologic therapies, microRNA-based therapies and mesenchymal stromal cell therapies, highlighting the pathophysiological basis and the influences on signal transduction pathways for their use.

[18] Benefits of animal models to understand the pathophysiology of depressive disorders.

  • Authors: B. Czéh, M. Simón
  • Year: 2020
  • Venue: Progress in neuro-psychopharmacology & biological psychiatry
  • URL: https://www.semanticscholar.org/paper/8caa4b74966abb2fe5b324dd454ebcb81a5f7b6a
  • DOI: 10.1016/j.pnpbp.2020.110049
  • PMID: 32735913
  • Citations: 24
  • Summary: It is argued, that despite their evident imperfections, these models provide invaluable help to understand cellular and molecular mechanisms contributing to the development of MDD.
  • Evidence snippets:
  • Snippet 1 (score: 0.436) > Based on our current understanding it appears that all major cell types of the CNS contribute to the pathophysiology of MDD. Both excitatory and inhibitory neurons, as well as the glial cells are involved, but we know very little about the sequence of events. The key questions are: Which cell type is the weakest link? Is there a specific cellular cascade mechanism leading to the pathophysiology, or all the cellular changes are taking place parallel to each other? It is still not clear whether all these cellular alterations are evidences of cellular "damage" or some of them represent compensatory mechanisms. Longitudinal studies focusing on several cell types simultaneously may yield answers to these questions. > Animal models for mental disorders received heavy criticisms and has been occasionally named as scapegoats for the lack of developments in psychiatric therapeutics. Despite all their significant shortcomings these models are extensively used in academic research and drug development. We should accept that none of the models can mimic all aspects of this complex disease, but they can provide opportunities to understand the specific genetic, molecular and cellular mechanisms contributing to the development of MDD.

[19] Navigating the disease landscape: knowledge representations for contextualizing molecular signatures

  • Authors: M. Saqi, A. Lysenko, Yi-Ke Guo, T. Tsunoda, C. Auffray
  • Year: 2018
  • Venue: Briefings in Bioinformatics
  • URL: https://www.semanticscholar.org/paper/70d6d85cc0f6f5fa4347d7a6135a322c81a41945
  • DOI: 10.1093/bib/bby025
  • PMID: 29684165
  • PMCID: 6556902
  • Citations: 14
  • Summary: This review discusses knowledge representations that can be useful to explore the biological context of molecular signatures, in particular three main approaches, namely, pathway mapping approaches, molecular network centric approaches and approaches that represent biological statements as knowledge graphs.
  • Evidence snippets:
  • Snippet 1 (score: 0.431) > Owing to technological advances allowing rapid and low-cost profiling of biological systems, multiple types of omics data are now routinely collected from patient cohorts in studies of human diseases. These data can lead to a new taxonomy of disease [1]. Diseases that were previously considered to be single homogeneous conditions may in fact be collections of several disease subtypes. Identification of subtypes allows targeting of the underlying molecular processes involved in the particular form of disease associated with the subtype, and can lead to more personalized therapeutic strategies. A major challenge for translational medicine informatics is the effective exploitation of these data types to develop a more complete picture of the disease, in particular a description of how changes at the molecular level are associated with the disease mechanism and disease pathophysiology. The molecular profiles by themselves do not, in general, offer immediate insight into the mechanism of disease or the underlying causes, and may be of limited utility for suggesting targets for therapeutic intervention. Putting these molecular patterns into a broader biological context represents a useful approach for understanding the underlying themes involved in the disease pathology, and this involves integrating the molecular profiles with other data types, including pathways, cellular and physiological data. > Together with data warehousing and data analytics, the contextualization of data emerging from high-throughput experiments is an important component of a translational informatics pipeline. The contextualization of experimental data is facilitated by mapping the data to background knowledge, which can include information at multiple levels of granularity. An effective representation of the disease needs to relate diseasespecific information to background knowledge so as to help researchers identify how dysfunctional proteins, pathways or other molecular processes lead to the cellular or physiological changes contributing to its aetiology. > Here, we review efforts to represent the context of diseaseimplicated genes, and we suggest that they can be divided into three broad themes, namely, pathway-centric, molecular network centric and approaches that represent biological statements as a knowledge graph (Table 1). We describe the advantages and drawbacks of the different representations. We do not discuss the details by which the genes are mapped to pathways or networks (for review of approaches to data interpretation, see for example [2]).

Notes

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