ArticleCell cycle (Georgetown, Tex.)2020
Globular adiponectin alleviates chronic intermittent hypoxia-induced H9C2 cardiomyocytes apoptosis via ER-phagy induction.
Article in Cell cycle (Georgetown, Tex.), 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 17 citations in OpenAlex.
- Organellophagy regulates cell death:A potential therapeutic target for inflammatory diseases.Journal of advanced research · 2025Review
- Ischemia-induced cardiac dysfunction is exacerbated in adiponectin-knockout mice due to impaired autophagy flux.Clinical and translational science · 2024Article
- Effects of obstructive sleep apnea on myocardial injury and dysfunction: a review focused on the molecular mechanisms of intermittent hypoxia.Sleep & breathing = Schlaf & Atmung · 2024Review
- Qingre Huoxue decoction attenuates myocardial ischemia‒reperfusion injury by regulating the autophagy‒endoplasmic reticulum stress axis via FAM134B-mediated ER-phagy.Frontiers in pharmacology · 2024Article
- PACS-2 deficiency aggravates tubular injury in diabetic kidney disease by inhibiting ER-phagy.Cell death & disease · 2023Article
- Endoplasmic Reticulum Selective Autophagy Alleviates Anthracycline-Induced Cardiotoxicity.JACC. CardioOncology · 2023Article
- Role of endoplasmic reticulum autophagy in acute lung injury.Frontiers in immunology · 2023Review
- Globular adiponectin protects hepatocytes against intermittent hypoxia-induced injury via Pink1/Parkin-mediated mitophagy induction.Sleep & breathing = Schlaf & Atmung · 2022Article
- ER-phagy: mechanisms, regulation, and diseases connected to the lysosomal clearance of the endoplasmic reticulum.Physiological reviews · 2022Review
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
This study evaluated the effects of endoplasmic reticulum autophagy (ER-phagy) and globular adiponectin (gAPN) on chronic intermittent hypoxia (CIH)-induced H9C2 cardiomyocytes injury while investigating potential mechanisms of action. The CIH model of H9C2 cardiomyocytes was established in this study. CCK-8 assay was used to determine cell viability post-exposure to various CIH times and gAPN concentrations. Flow cytometry was used to observe H9C2 cardiomyocytes apoptosis and immunofluorescence was used to measure ER-phagy and SEC62 activation. Western blot was used to observe ER stress and AMPK pathway. Results indicated that ER stress was activated in H9C2 cardiomyocytes exposed to CIH. Inhibition of ER stress reduced CIH-induced cell apoptosis. gAPN attenuated CIH-induced ER stress and H9C2 cardiomyocytes apoptosis. ER-phagy and SEC62 protein level were induced by CIH, while gAPN highly enhanced these changes. Inhibition of SEC62 expression reduced ER-phagy and increased ER stress and H9C2 cardiomyocytes apoptosis. Moreover, gAPN induced AMPK expression. Inhibition of AMPK expression reduced SEC62-mediated ER-phagy and increased the H9C2 cardiomyocytes apoptosis. Altogether, our study suggested that gAPN upregulated SEC62-mediated ER-phagy to extenuate ER stress, and mitigated H9C2 cardiomyocytes apoptosis induced by CIH through AMPK activation.
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