ArticleBMC pulmonary medicine2020
Attenuation of intermittent hypoxia-induced apoptosis and fibrosis in pulmonary tissues via suppression of ER stress activation.
Article in BMC pulmonary medicine, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers, 1 of them a synthesis that pooled it.
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Who cites it
21 citing papers in PubMed, 1 synthesis or guideline pooled it, 29 citations in OpenAlex.
- The impact of continuous positive airway pressure therapy on the recurrence of atrial fibrillation in patients with obstructive sleep apnea after pulmonary vein isolation.BMC cardiovascular disorders · 2025Pooled it
- Review
- The role of sleep disorders in orchestrating proteomic dysfunction and multi-morbidity.Molecular psychiatry · 2026Review
- PANoptosis as a drug discovery framework: integrating cell death architecture with clinical translation.Genes and immunity · 2026Review
- Single-cell landscape of mouse lungs exposed to intermittent hypoxia.Respiratory research · 2025Article
- [Aloe-emodin inhibits scar tissue fibrosis through thrombospondin-1-PI3k-Akt pathway].Hua xi kou qiang yi xue za zhi = Huaxi kouqiang yixue zazhi = West China journal of stomatology · 2025Article
- Interruption of intermittent hypoxia attenuates the severity of pulmonary fibrosis in male mice.Physiological reports · 2025Article
- Effects of Natural Products through Inhibiting Endoplasmic Reticulum Stress on Attenuation of Idiopathic Pulmonary Fibrosis.Drug design, development and therapy · 2024Review
- Article
- Intermittent Hypoxia-Induced Cardiomyocyte Death Is Mediated by HIF-1 Dependent MAM Disruption.Antioxidants (Basel, Switzerland) · 2022Article
- The substitution of SERCA2 redox cysteine 674 promotes pulmonary vascular remodeling by activating IRE1Acta pharmaceutica Sinica. B · 2022Article
- Thrombospondin-1 Signaling Through the Calreticulin/LDL Receptor Related Protein 1 Axis: Functions and Possible Roles in Glaucoma.Frontiers in cell and developmental biology · 2022Review
- The Discovery, Validation, and Function of Hypoxia-Related Gene Biomarkers for Obstructive Sleep Apnea.Frontiers in medicine · 2022Article
- Sleep Apnea in Idiopathic Pulmonary Fibrosis: A Molecular Investigation in an Experimental Model of Fibrosis and Intermittent Hypoxia.Life (Basel, Switzerland) · 2021Article
- Review
- TGF-β-induced α-SMA expression is mediated by C/EBPβ acetylation in human alveolar epithelial cells.Molecular medicine (Cambridge, Mass.) · 2021Article
- Analysis of Circulating Microvesicles Levels and Effects of Associated Factors in Elderly Patients With Obstructive Sleep Apnea.Frontiers in aging neuroscience · 2021Article
- Early Emergence of Adaptive Mechanisms Sustaining Ig Production: Application to Antibody Therapy.Frontiers in immunology · 2021Review
- Mechanism of Fei-Xian Formula in the Treatment of Pulmonary Fibrosis on the Basis of Network Pharmacology Analysis Combined with Molecular Docking Validation.Evidence-based complementary and alternative medicine : eCAM · 2021Article
- Management of Progressive Fibrosing Interstitial Lung Diseases (PF-ILD).Frontiers in medicine · 2021Review
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 1 country.
Funding
Abstract
backgroundObstructive sleep apnea (OSA) is associated with pulmonary fibrosis and endothelial apoptosis in pulmonary tissues. Chronic intermittent hypoxia (IH) is considered to be the primary player in OSA, but the mechanisms underlying its effect on pulmonary tissues are unknown. Endoplasmic reticulum (ER) stress induced by IH treatment plays an important role in accelerating the process of fibrosis and induction of apoptosis.
methodsMice were placed in IH chambers for 4 weeks with an oscillating oxygen (O
resultsAfter 4 weeks of IH treatment, the expressions of two ER stress markers, glucose regulated protein-78 (Grp78) and transcription factor C/EBP homologous protein (CHOP) were increased which was prevented by administration of the ER stress attenuator, TUDCA. The expressions of PERK, but not those of ATF-6 and IRE-1, were increased. The effects of IH were accompanied by an increased number of apoptotic cells and increased expressions of cleaved caspase-3 and caspase-12 in pulmonary tissues. In addition, histological examination suggested the presence of fibrosis after chronic IH treatment, indicated by increased expression of collagen, which was associated with the up-regulation of TGF-β1 and TSP-1 that are known to promote fibrosis. Similarly, TUDCA could reduce the extent of fibrotic area and the expression levels of these proteins.
conclusionsIt reveals the roles of ER stress, especially the PERK pathway, in IH induced apoptosis and fibrosis in pulmonary tissues that might underlie the pulmonary complications observed in OSA.
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