ArticlePloS one2016
HO-1 Protects against Hypoxia/Reoxygenation-Induced Mitochondrial Dysfunction in H9c2 Cardiomyocytes.
Article in PloS one, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 36 citations in OpenAlex.
- Passive heat therapy protects against endothelial cell hypoxia-reoxygenation via effects of elevations in temperature and circulating factors.The Journal of physiology · 2018Trial
- GPR40-full agonist AM1638 alleviates palmitate-induced oxidative damage in H9c2 cells via an AMPK-dependent pathway.BMB reports · 2025Article
- Bacterial endotoxin-lipopolysaccharide role in inflammatory diseases: An overview.Iranian journal of basic medical sciences · 2025Review
- Protective effect of Pinacidil on hypoxic-reoxygenated cardiomyocytes in vitro and in vivo via HIF-1α/HRE pathway.PloS one · 2025Article
- Allicin protects against LPS-induced cardiomyocyte injury by activating Nrf2-HO-1 and inhibiting NLRP3 pathways.BMC cardiovascular disorders · 2023Article
- Regulation of autophagy of the heart in ischemia and reperfusion.Apoptosis : an international journal on programmed cell death · 2023Review
- Platelet Membrane-Encapsulated MSNs Loaded with SS31 Peptide Alleviate Myocardial Ischemia-Reperfusion Injury.Journal of functional biomaterials · 2022Article
- Mitochondrial Damage in Myocardial Ischemia/Reperfusion Injury and Application of Natural Plant Products.Oxidative medicine and cellular longevity · 2022Review
- Adiponectin inhibits D‑gal‑induced cardiomyocyte senescence via AdipoR1/APPL1.Molecular medicine reports · 2021Article
- Oxidative Stress in Ischemic Heart Disease.Oxidative medicine and cellular longevity · 2020Review
- Sirtuin1 Role in the Melatonin Protective Effects Against Obesity-Related Heart Injury.Frontiers in physiology · 2020Article
- The Nrf-2/HO-1 Signaling Axis: A Ray of Hope in Cardiovascular Diseases.Cardiology research and practice · 2020Review
- Identification of potential molecular mechanisms and small molecule drugs in myocardial ischemia/reperfusion injury.Brazilian journal of medical and biological research = Revista brasileira de pesquisas medicas e biologica · 2020Article
- Shexiang Tongxin Dropping Pill () Protects against NaChinese journal of integrative medicine · 2019Article
- Apurinic/apyrimidinic endonuclease/redox factor 1 (APE1) alleviates myocardial hypoxia-reoxygenation injury by inhibiting oxidative stress and ameliorating mitochondrial dysfunction.Experimental and therapeutic medicine · 2019Article
- Heme oxygenase-1 ameliorates hypoxia/reoxygenation via suppressing apoptosis and enhancing autophagy and cell proliferation though Sirt3 signaling pathway in H9c2 cells.Naunyn-Schmiedeberg's archives of pharmacology · 2019Article
- Carnosic Acid as a Promising Agent in Protecting Mitochondria of Brain Cells.Molecular neurobiology · 2018Review
- SB202190 inhibits endothelial cell apoptosis via induction of autophagy and heme oxygenase-1.Oncotarget · 2018Article
- Potential signaling pathways of acute endurance exercise-induced cardiac autophagy and mitophagy and its possible role in cardioprotection.The journal of physiological sciences : JPS · 2017Review
- CLOCK Promotes Endothelial Damage by Inducing Autophagy through Reactive Oxygen Species.Oxidative medicine and cellular longevity · 2016Article
Corrections and comments
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Authors and funding
9 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundMitochondrial dysfunction would ultimately lead to myocardial cell apoptosis and death during ischemia-reperfusion injuries. Autophagy could ameliorate mitochondrial dysfunction by autophagosome forming, which is a catabolic process to preserve the mitochondrial's structural and functional integrity. HO-1 induction and expression are important protective mechanisms. This study in order to investigate the role of HO-1 during mitochondrial damage and its mechanism. METHODS AND
resultsThe H9c2 cardiomyocyte cell line were incubated by hypoxic and then reoxygenated for the indicated time (2, 6, 12, 18, and 24 h). Cell viability was tested with CCK-8 kit. The expression of endogenous HO-1(RT-PCR and Western blot) increased with the duration of reoxygenation and reached maximum levels after 2 hours of H/R; thereafter, the expression gradually decreased to a stable level. Mitochondrial dysfunction (Flow cytometry quantified the ROS generation and JC-1 staining) and autophagy (The Confocal microscopy measured the autophagy. RFP-GFP-LC3 double-labeled adenovirus was used for testing.) were induced after 6 hours of H/R. Then, genetic engineering technology was employed to construct an Lv-HO1-H9c2 cell line. When HO-1 was overexpressed, the LC3II levels were significantly increased after reoxygenation, p62 protein expression was significantly decreased, the level of autophagy was unchanged, the mitochondrial membrane potential was significantly increased, and the mitochondrial ROS level was significantly decreased. Furthermore, when the HO-1 inhibitor ZnPP was applied the level of autophagy after reoxygenation was significantly inhibited, and no significant improvement in mitochondrial dysfunction was observed.
conclusionsDuring myocardial hypoxia-reoxygenation injury, HO-1 overexpression induces autophagy to protect the stability of the mitochondrial membrane and reduce the amount of mitochondrial oxidation products, thereby exerting a protective effect.
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