Obstructive Sleep Apnea

Pathophysiology description OSA is characterized by recurrent upper-airway collapse during sleep, producing cycles of intermittent hypoxia and reoxygenation and sleep fragmentation. These cycles stabilize HIF‑1α, increase reactive oxygen species (ROS) via NADPH oxidases, activate NF‑κB–dependent inflammation, decrease endothelial nitric oxide (NO) bioavailability, and drive sympathetic overactivity, collectively promoting endothelial dysfunction, vascular remodeling, metabolic dysregulation, and neurocognitive injury (https://doi.org/10.3390/life14040425, Mar 22, 2024) (lavalle2024unravelingthecomplexities pages 1-2, lavalle2024unravelingthecomplexities pages 6-8, lavalle2024unravelingthecomplexities pages 2-3). A recent meta-analysis of rodent intermittent hypoxia (IH), an established OSA model, demonstrates robust increases in cerebral oxidative stress (↑MDA, ↑NADPH oxidase), inflammation (↑TNF‑α, ↑NF‑κB, ↑iNOS), HIF‑1, and apoptosis (↑TUNEL, ↑cleaved caspase‑3), linking IH to brain injury (https://doi.org/10.1183/16000617.0162-2024, Oct 2024) (amine2024cerebraloxidativestress pages 1-2). Clinically, OSA is associated with hypertension, arrhythmias, coronary disease, heart failure, and neurocognitive impairment; sympathetic surges and intrathoracic pressure swings further contribute to cardiovascular stress, while CPAP reliably reduces apneas though cardioprotective effects are inconsistent across endpoints (https://doi.org/10.3390/life14040425, 2024; https://doi.org/10.3390/biomedicines12112503, Nov 2024) (lavalle2024unravelingthecomplexities pages 10-12, karakasis2024mitigatingincreasedcardiovascular pages 4-5).

1) Core Pathophysiology - Intermittent hypoxia/reoxygenation and oxidative stress: IH stabilizes HIF‑1α and augments ROS generation (notably via NADPH oxidase), leading to lipid peroxidation, protein/DNA oxidation, mitochondrial dysfunction, and activation of MAPKs and MMPs; ROS also react with NO to form peroxynitrite, intensifying nitrosative stress (https://doi.org/10.3390/life14040425, 2024) (lavalle2024unravelingthecomplexities pages 6-8). - Systemic and endothelial inflammation: IH and ROS activate NF‑κB, upregulating TNF‑α, IL‑6, IL‑8, and adhesion molecules (E‑selectin, VCAM‑1, ICAM‑1), fostering leukocyte recruitment and endothelial activation (https://doi.org/10.3390/life14040425, 2024) (lavalle2024unravelingthecomplexities pages 9-10, lavalle2024unravelingthecomplexities pages 8-9). - Endothelial dysfunction: Reduced NO bioavailability (eNOS inhibition/ADMA, NO scavenging by superoxide) and increased vasoconstrictors impair vasodilation and accelerate atherogenesis (https://doi.org/10.3390/life14040425, 2024) (lavalle2024unravelingthecomplexities pages 8-9, lavalle2024unravelingthecomplexities pages 9-10). - Autonomic/sympathetic activation: Chemoreflex activation by IH elevates sympathetic tone, producing blood pressure surges and sustained nocturnal hypertension; endothelial dysfunction and prothrombotic pathways add cardiovascular risk (https://doi.org/10.3390/biomedicines12112503, 2024) (karakasis2024mitigatingincreasedcardiovascular pages 4-5, lavalle2024unravelingthecomplexities pages 10-12). - Upper airway collapsibility and neuromuscular control: Sleep-related reduction in dilator muscle drive (e.g., genioglossus) and pharyngeal anatomy increase collapsibility; phenotypic treatment approaches emphasize these endotypes (reviewed) (https://doi.org/10.3390/ijms24065478, Mar 13, 2023) (meliante2023molecularpathologyoxidative pages 1-2). - Ventilatory control instability (loop gain): Respiratory control abnormalities interact with collapsibility to perpetuate apnea cycles; IH amplifies chemoreflex sensitivity (reviewed) (https://doi.org/10.3390/ijms24065478, 2023) (meliante2023molecularpathologyoxidative pages 1-2). - Metabolic dysregulation: OSA-related hypoxemia is linked to oxidative stress, systemic inflammation, and altered antioxidant defenses (↓GSH, ↓SOD, ↓vitamin E), mechanistically tied to insulin resistance and dyslipidemia (https://doi.org/10.3390/life14040425, 2024; https://doi.org/10.3390/ijms24065478, 2023) (lavalle2024unravelingthecomplexities pages 5-6, meliante2023molecularpathologyoxidative pages 1-2). - Neurocognitive/cerebrovascular injury: IH induces cerebral oxidative stress, inflammation, HIF‑1 upregulation, and apoptosis, supporting mechanistic links to cognitive impairment (https://doi.org/10.1183/16000617.0162-2024, 2024) (amine2024cerebraloxidativestress pages 1-2).

2) Key Molecular Players - Genes/proteins (HGNC): HIF1A (hypoxia sensor) (meliante2023molecularpathologyoxidative pages 1-2); NFKB1 (inflammatory TF) (lavalle2024unravelingthecomplexities pages 2-3, lavalle2024unravelingthecomplexities pages 8-9); CYBB/NOX2 (NADPH oxidase; superoxide source) (lavalle2024unravelingthecomplexities pages 6-8); NOS3/eNOS (endothelial NO synthase; reduced NO bioavailability) (lavalle2024unravelingthecomplexities pages 9-10, lavalle2024unravelingthecomplexities pages 8-9); EDN1/ET‑1 (vasoconstrictor; vascular stress) (lavalle2024unravelingthecomplexities pages 8-9); IL6 and TNF (proinflammatory cytokines; correlate with severity) (lavalle2024unravelingthecomplexities pages 9-10, lavalle2024unravelingthecomplexities pages 2-3). See artifact table below for concise ontology mappings. - Chemical entities (CHEBI): ROS, superoxide (O2•–), nitric oxide (NO), peroxynitrite (ONOO–), ADMA (endogenous NOS inhibitor) (lavalle2024unravelingthecomplexities pages 6-8, lavalle2024unravelingthecomplexities pages 8-9, lavalle2024unravelingthecomplexities pages 9-10). - Cell types (CL): Vascular endothelial cells, neutrophils, monocytes/macrophages, astrocytes, microglia, neurons, cardiomyocytes (lavalle2024unravelingthecomplexities pages 9-10, amine2024cerebraloxidativestress pages 1-2, lavalle2024unravelingthecomplexities pages 10-12). - Anatomical locations (UBERON): Upper respiratory tract/pharynx, soft palate, tongue/genioglossus (airway patency), vascular endothelium, brain/hippocampus ( not available; supported generally by 2023–2024 reviews above) (meliante2023molecularpathologyoxidative pages 1-2, amine2024cerebraloxidativestress pages 1-2, lavalle2024unravelingthecomplexities pages 9-10).

Table: Concise ontology-annotated table linking key genes, chemicals, cell types, anatomical sites and GO processes to their roles in OSA pathophysiology, with supporting evidence citations (lavalle2024unravelingthecomplexities pages 10-12, lavalle2024unravelingthecomplexities pages 1-2).

3) Biological Processes (GO terms) - Response to hypoxia (GO:0001666): IH stabilizes HIF‑1α and reprograms metabolism and angiogenesis; links hypoxia sensing to downstream injury (meliante2023molecularpathologyoxidative pages 1-2, lavalle2024unravelingthecomplexities pages 6-8). - Response to oxidative stress (GO:0006979): ROS accumulation from NOX and mitochondria drives lipid peroxidation, protein/DNA damage, and signaling cascades (lavalle2024unravelingthecomplexities pages 6-8, lavalle2024unravelingthecomplexities pages 5-6). - Inflammatory response and NF‑κB signaling (GO:0006954; GO:0038061): IH/ROS activate NF‑κB, elevating TNF‑α, IL‑6, IL‑8 and adhesion molecules (lavalle2024unravelingthecomplexities pages 8-9, lavalle2024unravelingthecomplexities pages 9-10, lavalle2024unravelingthecomplexities pages 2-3). - Nitric oxide biosynthetic process (GO:0006809): eNOS-derived NO is reduced by ADMA and ROS scavenging, impairing vasodilation (lavalle2024unravelingthecomplexities pages 8-9, lavalle2024unravelingthecomplexities pages 9-10). - Endothelial cell apoptosis (GO:0072577): ROS and peroxynitrite trigger endothelial injury and apoptosis, advancing vascular remodeling (lavalle2024unravelingthecomplexities pages 6-8, lavalle2024unravelingthecomplexities pages 8-9).

4) Cellular Components - Plasma membrane/caveolae and endothelium: NO/eNOS signaling, adhesion molecule expression, oxidant interactions (lavalle2024unravelingthecomplexities pages 9-10, lavalle2024unravelingthecomplexities pages 8-9). - Mitochondria: ROS generation/dysfunction during IH–reoxygenation (lavalle2024unravelingthecomplexities pages 6-8). - Cytosol/nucleus: NF‑κB activation and HIF‑1α transcriptional programs (lavalle2024unravelingthecomplexities pages 2-3, lavalle2024unravelingthecomplexities pages 6-8). - Extracellular space: Cytokines (TNF‑α, IL‑6), NO/NOx, ADMA, adhesion events (lavalle2024unravelingthecomplexities pages 9-10, lavalle2024unravelingthecomplexities pages 8-9).

5) Disease Progression (sequence of events) - Upper-airway collapsibility during sleep → recurrent apneas/hypopneas → IH/reoxygenation and sleep fragmentation → HIF‑1α stabilization and ROS bursts (NOX/mitochondria) → NF‑κB–driven inflammation and reduced NO bioavailability (ADMA, NO scavenging) → endothelial activation (CAMs), dysfunction, vasoconstriction, and sympathetic surges → vascular remodeling, hypertension, atherogenesis, arrhythmogenic substrate; in brain, IH elevates NOX, TNF‑α, NF‑κB and apoptosis markers → cognitive impairment (https://doi.org/10.3390/life14040425, 2024; https://doi.org/10.1183/16000617.0162-2024, 2024) (lavalle2024unravelingthecomplexities pages 6-8, amine2024cerebraloxidativestress pages 1-2, lavalle2024unravelingthecomplexities pages 9-10).

6) Phenotypic Manifestations (selected HP terms) - Excessive daytime sleepiness (HP:0001254), non-restorative sleep; witnessed apneas/snoring; nocturnal hypoxemia. - Hypertension, notably resistant or nocturnal non-dipping patterns; endothelial dysfunction and increased arterial stiffness (https://doi.org/10.3390/biomedicines12112503, 2024; https://doi.org/10.3390/life14040425, 2024) (karakasis2024mitigatingincreasedcardiovascular pages 4-5, lavalle2024unravelingthecomplexities pages 8-9). - Cardiovascular: coronary artery disease, heart failure, atrial fibrillation; cerebrovascular/cognitive impairment linked to IH-induced brain inflammation/oxidative stress (https://doi.org/10.1183/16000617.0162-2024, 2024) (amine2024cerebraloxidativestress pages 1-2, lavalle2024unravelingthecomplexities pages 10-12).

Recent developments (prioritized 2023–2024) and expert perspectives - Oxidative stress and inflammatory biomarker synthesis: A 2024 comprehensive review collates redox and inflammatory biomarkers in OSA and emphasizes endothelial dysfunction as an early, central lesion; it also highlights inconsistent biomarker standardization and the potential but as-yet unproven benefit of antioxidant adjuncts (https://doi.org/10.3390/life14040425, Mar 22, 2024) (lavalle2024unravelingthecomplexities pages 1-2, lavalle2024unravelingthecomplexities pages 8-9). - Brain-focused IH meta-analysis: 2024 ERS review/meta-analysis confirms IH causally increases brain oxidative stress, inflammation, HIF‑1, and apoptosis across rodent paradigms, strengthening mechanistic plausibility of OSA-related neurocognitive injury (https://doi.org/10.1183/16000617.0162-2024, Oct 2024) (amine2024cerebraloxidativestress pages 1-2). - Cardiovascular/autonomic integration: 2024 review details sympathetic activation, chemoreflex sensitization, endothelial injury, and potential contributions of renin–angiotensin–aldosterone activation in mediating BP surges and persistent nocturnal hypertension; it also discusses emerging cardiometabolic pharmacotherapies (GLP‑1RA, SGLT2i) as adjuncts to improve risk profiles in OSA (https://doi.org/10.3390/biomedicines12112503, Nov 2024) (karakasis2024mitigatingincreasedcardiovascular pages 4-5). - Molecular pathology: A 2023 review synthesizes IH-driven HIF‑1α and ROS pathways, linking to systemic inflammation and endothelial dysfunction, and notes CPAP reverses many molecular alterations while pharmacologic candidates (e.g., antioxidants, neuromodulators) remain investigational (https://doi.org/10.3390/ijms24065478, Mar 13, 2023) (meliante2023molecularpathologyoxidative pages 1-2).

Current applications and real-world implementations - CPAP: Effective at eliminating obstructive events and improving sleepiness; its consistent impact on secondary cardiovascular endpoints remains mixed, underscoring the need for phenotype‑ and mechanism‑guided adjuncts (https://doi.org/10.3390/life14040425, 2024) (lavalle2024unravelingthecomplexities pages 10-12). - Precision phenotyping/endotyping: Targeting anatomic (pharyngeal structure, soft palate, tongue) and non‑anatomic traits (dilator muscle responsiveness, loop gain, arousal threshold) guides use of mandibular advancement devices, positional therapy, hypoglossal nerve stimulation, or pharmacologic neuromodulators (reviewed) (https://doi.org/10.3390/ijms24065478, 2023) (meliante2023molecularpathologyoxidative pages 1-2). - Cardiometabolic pharmacotherapies: GLP‑1 receptor agonists and SGLT2 inhibitors may improve weight, BP, endothelial function, and inflammation, potentially reducing OSA severity and cardiovascular risk; definitive outcome trials in OSA populations are needed (https://doi.org/10.3390/biomedicines12112503, 2024) (karakasis2024mitigatingincreasedcardiovascular pages 4-5).

Relevant statistics and quantitative data - Global burden: OSA affects “approximately 1 billion adults globally,” emphasizing high public health impact (https://doi.org/10.3390/life14040425, 2024) (lavalle2024unravelingthecomplexities pages 1-2). - Resistant hypertension: Up to 80% of resistant hypertension cases may have coexisting OSA, underscoring the strong association and the role of sympathetic activation and endothelial injury (https://doi.org/10.3390/life14040425, 2024) (lavalle2024unravelingthecomplexities pages 10-12). - Oxidative/antioxidant imbalance: Reported reductions in antioxidant defenses include decreased total GSH (OSAS mean 0.389–0.449 nmol/μL vs 0.574–0.713 nmol/μL in controls; p<0.0001), altered GSH/GSSG ratio (p=0.03), reduced vitamin E (p<0.006) and SOD (p<0.001), and increased homocysteine (p<0.02), supporting systemic oxidative stress (https://doi.org/10.3390/life14040425, 2024) (lavalle2024unravelingthecomplexities pages 5-6, lavalle2024unravelingthecomplexities pages 8-9).

Direct quotes supporting key statements - “The cyclic pattern of intermittent hypoxia in OSAS triggers oxidative stress” and “triggers arterial chemoreceptors, heightening sympathetic nervous system activity,” linking ROS and autonomic activation (https://doi.org/10.3390/life14040425, 2024) (lavalle2024unravelingthecomplexities pages 1-2). - IH “stabilizes and accumulates [HIF‑1α], triggering the transcription of various genes” and NOX “convert[s] free oxygen (O2) into superoxide,” anchoring hypoxia-oxidative pathways (https://doi.org/10.3390/life14040425, 2024) (lavalle2024unravelingthecomplexities pages 6-8). - IH in rodents “robustly establishes” increased cerebral oxidative stress, inflammation, HIF‑1, and apoptosis, implicating brain vulnerability to OSA (https://doi.org/10.1183/16000617.0162-2024, 2024) (amine2024cerebraloxidativestress pages 1-2).

Structured annotations for knowledge base - Gene/protein annotations (HGNC): HIF1A; NFKB1; CYBB (NOX2); NOS3 (eNOS); EDN1 (ET‑1); IL6; TNF (lavalle2024unravelingthecomplexities pages 6-8, lavalle2024unravelingthecomplexities pages 9-10, lavalle2024unravelingthecomplexities pages 2-3, lavalle2024unravelingthecomplexities pages 8-9, meliante2023molecularpathologyoxidative pages 1-2). - GO biological processes: response to hypoxia (GO:0001666); response to oxidative stress (GO:0006979); inflammatory response (GO:0006954); NF‑κB signaling (GO:0038061); nitric oxide biosynthetic process (GO:0006809); endothelial cell apoptosis (GO:0072577) (lavalle2024unravelingthecomplexities pages 6-8, lavalle2024unravelingthecomplexities pages 2-3, lavalle2024unravelingthecomplexities pages 8-9). - Cellular components: endothelium/plasma membrane (eNOS/adhesion molecule signaling), mitochondria (ROS), cytosol/nucleus (HIF‑1α/NF‑κB), extracellular space (cytokines/NO/ADMA) (lavalle2024unravelingthecomplexities pages 9-10, lavalle2024unravelingthecomplexities pages 6-8, lavalle2024unravelingthecomplexities pages 8-9). - Cell types (CL): endothelial cells, neutrophils, monocytes/macrophages, astrocytes, microglia, neurons, cardiomyocytes (lavalle2024unravelingthecomplexities pages 9-10, amine2024cerebraloxidativestress pages 1-2, lavalle2024unravelingthecomplexities pages 10-12). - Anatomical locations (UBERON): upper respiratory tract/pharynx, soft palate, tongue/genioglossus, vascular endothelium, brain/hippocampus (meliante2023molecularpathologyoxidative pages 1-2, amine2024cerebraloxidativestress pages 1-2, lavalle2024unravelingthecomplexities pages 9-10). - Chemical entities (CHEBI): ROS, superoxide, NO, peroxynitrite, ADMA (lavalle2024unravelingthecomplexities pages 6-8, lavalle2024unravelingthecomplexities pages 8-9).

Evidence items (with PMIDs if available; DOIs/URLs provided above) - Lavalle et al., 2024 (Life; DOI:10.3390/life14040425) – oxidative stress/inflammation, endothelial dysfunction, sympathetic activation, prevalence statistics (lavalle2024unravelingthecomplexities pages 1-2, lavalle2024unravelingthecomplexities pages 8-9, lavalle2024unravelingthecomplexities pages 2-3, lavalle2024unravelingthecomplexities pages 5-6, lavalle2024unravelingthecomplexities pages 6-8, lavalle2024unravelingthecomplexities pages 9-10). - Amine et al., 2024 (Eur Respir Rev; DOI:10.1183/16000617.0162-2024) – IH meta-analysis demonstrating cerebral oxidative stress, inflammation, HIF‑1, apoptosis (amine2024cerebraloxidativestress pages 1-2). - Karakasis et al., 2024 (Biomedicines; DOI:10.3390/biomedicines12112503) – cardiovascular/autonomic mechanisms, endothelial dysfunction, pharmaco-adjuncts (karakasis2024mitigatingincreasedcardiovascular pages 4-5). - Meliante et al., 2023 (Int J Mol Sci; DOI:10.3390/ijms24065478) – molecular pathology overview, roles for IH, ROS, NF‑κB, endothelial dysfunction; therapeutic notes (meliante2023molecularpathologyoxidative pages 1-2).

Expert analysis The mechanistic framework converges on IH→ROS/HIF‑1α→NF‑κB/inflammation→endothelial dysfunction and sympathetic activation. These processes plausibly explain the multi-organ phenotype of OSA and its cardiometabolic and neurocognitive sequelae. Animal-model meta-analysis provides strong causality for brain injury pathways under IH. Clinically, addressing the anatomical endotype (collapsibility) with CPAP/oral devices/nerve stimulation remains foundational, while cardiometabolic risk may require adjunctive strategies (weight loss, GLP‑1RA/SGLT2i). Biomarker standardization and interventional trials targeting redox/inflammatory axes are priority gaps (amine2024cerebraloxidativestress pages 1-2, karakasis2024mitigatingincreasedcardiovascular pages 4-5, lavalle2024unravelingthecomplexities pages 8-9).

References

1. (lavalle2024unravelingthecomplexities pages 1-2): Salvatore Lavalle, Edoardo Masiello, Giannicola Iannella, Giuseppe Magliulo, Annalisa Pace, Jerome Rene Lechien, Christian Calvo-Henriquez, Salvatore Cocuzza, Federica Maria Parisi, Valentin Favier, Ahmed Yassin Bahgat, Giovanni Cammaroto, Luigi La Via, Caterina Gagliano, Alberto Caranti, Claudio Vicini, and Antonino Maniaci. Unraveling the complexities of oxidative stress and inflammation biomarkers in obstructive sleep apnea syndrome: a comprehensive review. Life, 14:425, Mar 2024. URL: https://doi.org/10.3390/life14040425, doi:10.3390/life14040425. This article has 83 citations and is from a poor quality or predatory journal.

2. (lavalle2024unravelingthecomplexities pages 6-8): Salvatore Lavalle, Edoardo Masiello, Giannicola Iannella, Giuseppe Magliulo, Annalisa Pace, Jerome Rene Lechien, Christian Calvo-Henriquez, Salvatore Cocuzza, Federica Maria Parisi, Valentin Favier, Ahmed Yassin Bahgat, Giovanni Cammaroto, Luigi La Via, Caterina Gagliano, Alberto Caranti, Claudio Vicini, and Antonino Maniaci. Unraveling the complexities of oxidative stress and inflammation biomarkers in obstructive sleep apnea syndrome: a comprehensive review. Life, 14:425, Mar 2024. URL: https://doi.org/10.3390/life14040425, doi:10.3390/life14040425. This article has 83 citations and is from a poor quality or predatory journal.

3. (lavalle2024unravelingthecomplexities pages 2-3): Salvatore Lavalle, Edoardo Masiello, Giannicola Iannella, Giuseppe Magliulo, Annalisa Pace, Jerome Rene Lechien, Christian Calvo-Henriquez, Salvatore Cocuzza, Federica Maria Parisi, Valentin Favier, Ahmed Yassin Bahgat, Giovanni Cammaroto, Luigi La Via, Caterina Gagliano, Alberto Caranti, Claudio Vicini, and Antonino Maniaci. Unraveling the complexities of oxidative stress and inflammation biomarkers in obstructive sleep apnea syndrome: a comprehensive review. Life, 14:425, Mar 2024. URL: https://doi.org/10.3390/life14040425, doi:10.3390/life14040425. This article has 83 citations and is from a poor quality or predatory journal.

4. (amine2024cerebraloxidativestress pages 1-2): Bayan El Amine, Joey Fournier, Mélanie Minoves, Sébastien Baillieul, Frédéric Roche, Nathalie Perek, Jean-Louis Pépin, Renaud Tamisier, Charles Khouri, Claire Rome, and Anne Briançon-Marjollet. Cerebral oxidative stress, inflammation and apoptosis induced by intermittent hypoxia: a systematic review and meta-analysis of rodent data. European Respiratory Review, 33:240162, Oct 2024. URL: https://doi.org/10.1183/16000617.0162-2024, doi:10.1183/16000617.0162-2024. This article has 7 citations and is from a peer-reviewed journal.

5. (lavalle2024unravelingthecomplexities pages 10-12): Salvatore Lavalle, Edoardo Masiello, Giannicola Iannella, Giuseppe Magliulo, Annalisa Pace, Jerome Rene Lechien, Christian Calvo-Henriquez, Salvatore Cocuzza, Federica Maria Parisi, Valentin Favier, Ahmed Yassin Bahgat, Giovanni Cammaroto, Luigi La Via, Caterina Gagliano, Alberto Caranti, Claudio Vicini, and Antonino Maniaci. Unraveling the complexities of oxidative stress and inflammation biomarkers in obstructive sleep apnea syndrome: a comprehensive review. Life, 14:425, Mar 2024. URL: https://doi.org/10.3390/life14040425, doi:10.3390/life14040425. This article has 83 citations and is from a poor quality or predatory journal.

6. (karakasis2024mitigatingincreasedcardiovascular pages 4-5): Paschalis Karakasis, Marios Sagris, Dimitrios Patoulias, Theocharis Koufakis, Panagiotis Theofilis, Aleksandra Klisic, Nikolaos Fragakis, Mohamed El Tanani, and Manfredi Rizzo. Mitigating increased cardiovascular risk in patients with obstructive sleep apnea using glp-1 receptor agonists and sglt2 inhibitors: hype or hope? Biomedicines, 12:2503, Nov 2024. URL: https://doi.org/10.3390/biomedicines12112503, doi:10.3390/biomedicines12112503. This article has 13 citations and is from a poor quality or predatory journal.

7. (lavalle2024unravelingthecomplexities pages 9-10): Salvatore Lavalle, Edoardo Masiello, Giannicola Iannella, Giuseppe Magliulo, Annalisa Pace, Jerome Rene Lechien, Christian Calvo-Henriquez, Salvatore Cocuzza, Federica Maria Parisi, Valentin Favier, Ahmed Yassin Bahgat, Giovanni Cammaroto, Luigi La Via, Caterina Gagliano, Alberto Caranti, Claudio Vicini, and Antonino Maniaci. Unraveling the complexities of oxidative stress and inflammation biomarkers in obstructive sleep apnea syndrome: a comprehensive review. Life, 14:425, Mar 2024. URL: https://doi.org/10.3390/life14040425, doi:10.3390/life14040425. This article has 83 citations and is from a poor quality or predatory journal.

8. (lavalle2024unravelingthecomplexities pages 8-9): Salvatore Lavalle, Edoardo Masiello, Giannicola Iannella, Giuseppe Magliulo, Annalisa Pace, Jerome Rene Lechien, Christian Calvo-Henriquez, Salvatore Cocuzza, Federica Maria Parisi, Valentin Favier, Ahmed Yassin Bahgat, Giovanni Cammaroto, Luigi La Via, Caterina Gagliano, Alberto Caranti, Claudio Vicini, and Antonino Maniaci. Unraveling the complexities of oxidative stress and inflammation biomarkers in obstructive sleep apnea syndrome: a comprehensive review. Life, 14:425, Mar 2024. URL: https://doi.org/10.3390/life14040425, doi:10.3390/life14040425. This article has 83 citations and is from a poor quality or predatory journal.

9. (meliante2023molecularpathologyoxidative pages 1-2): Piero Giuseppe Meliante, Federica Zoccali, Francesca Cascone, Vanessa Di Stefano, Antonio Greco, Marco de Vincentiis, Carla Petrella, Marco Fiore, Antonio Minni, and Christian Barbato. Molecular pathology, oxidative stress, and biomarkers in obstructive sleep apnea. International Journal of Molecular Sciences, 24:5478, Mar 2023. URL: https://doi.org/10.3390/ijms24065478, doi:10.3390/ijms24065478. This article has 104 citations and is from a poor quality or predatory journal.

10. (lavalle2024unravelingthecomplexities pages 5-6): Salvatore Lavalle, Edoardo Masiello, Giannicola Iannella, Giuseppe Magliulo, Annalisa Pace, Jerome Rene Lechien, Christian Calvo-Henriquez, Salvatore Cocuzza, Federica Maria Parisi, Valentin Favier, Ahmed Yassin Bahgat, Giovanni Cammaroto, Luigi La Via, Caterina Gagliano, Alberto Caranti, Claudio Vicini, and Antonino Maniaci. Unraveling the complexities of oxidative stress and inflammation biomarkers in obstructive sleep apnea syndrome: a comprehensive review. Life, 14:425, Mar 2024. URL: https://doi.org/10.3390/life14040425, doi:10.3390/life14040425. This article has 83 citations and is from a poor quality or predatory journal.