ArticleScientific reports2016
Cardiac Specific Overexpression of Mitochondrial Omi/HtrA2 Induces Myocardial Apoptosis and Cardiac Dysfunction.
Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed, 46 citations in OpenAlex.
- Ovarian ageing: from biological constraint to emerging therapeutic frontier.Journal of assisted reproduction and genetics · 2026Review
- Gonadal transdifferentiation in teleosts during normal and altered physiology-a review.Fish physiology and biochemistry · 2026Review
- Anthracycline-induced cardiomyopathy in childhood cancer survivors is associated with gene signatures of mitochondrial dysfunction-a COG ALTE03N1 report.Cardio-oncology (London, England) · 2025Article
- Diminazine protects against cardiac aging through the improvement of mitophagy and apoptosis in aging rats induced by D-galactose.BMC cardiovascular disorders · 2025Article
- UPRmt-regulated mitokines: novel strategies for myocardial injury repair.Frontiers in cell and developmental biology · 2025Review
- Mitochondrial dysfunction at the crossroad of cardiovascular diseases and cancer.Journal of translational medicine · 2023Review
- Protease-independent control of parthanatos by HtrA2/Omi.Cellular and molecular life sciences : CMLS · 2023Article
- The Journey of Mitochondrial Protein Import and the Roadmap to Follow.International journal of molecular sciences · 2023Review
- Mitochondrial Omi/HtrA2 signaling pathway is involved in neuronal apoptosis in patients with cerebral hemorrhage.American journal of translational research · 2023Article
- Mitochondrial Protein Homeostasis and Cardiomyopathy.International journal of molecular sciences · 2022Review
- Omi inhibition ameliorates neuron apoptosis and neurological deficit after subarachnoid hemorrhage in rats.Genes & genomics · 2021Article
- Prevention of acquired sensorineural hearing loss in mice by in vivo Htra2 gene editing.Genome biology · 2021Article
- Nicorandil inhibits cardiomyocyte apoptosis and improves cardiac function by suppressing the HtrA2/XIAP/PARP signaling after coronary microembolization in rats.Pharmacology research & perspectives · 2021Article
- Protective Effect of Fasudil on Hydrogen Peroxide-Induced Oxidative Stress Injury of H9C2 Cardiomyocytes.Disease markers · 2021Article
- Mitochondrial Chaperones and Proteases in Cardiomyocytes and Heart Failure.Frontiers in molecular biosciences · 2021Review
- miR-16-5p Regulates PTPN4 and Affects Cardiomyocyte Apoptosis and Autophagy Induced by Hypoxia/Reoxygenation.Evidence-based complementary and alternative medicine : eCAM · 2021Article
- Mitochondrial unfolded protein response, mitophagy and other mitochondrial quality control mechanisms in heart disease and aged heart.Croatian medical journal · 2020Review
- Extracellular HtrA2 Induces Apoptosis in Human Umbilical Vein Endothelial Cells.International journal of molecular sciences · 2019Article
- Article
- miR-181c-5p Exacerbates Hypoxia/Reoxygenation-Induced Cardiomyocyte Apoptosis via Targeting PTPN4.Oxidative medicine and cellular longevity · 2019Article
Corrections and comments
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Authors and funding
12 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Myocardial apoptosis is a significant problem underlying ischemic heart disease. We previously reported significantly elevated expression of cytoplasmic Omi/HtrA2, triggers cardiomyocytes apoptosis. However, whether increased Omi/HtrA2 within mitochondria itself influences myocardial survival in vivo is unknown. We aim to observe the effects of mitochondria-specific, not cytoplasmic, Omi/HtrA2 on myocardial apoptosis and cardiac function. Transgenic mice overexpressing cardiac-specific mitochondrial Omi/HtrA2 were generated and they had increased myocardial apoptosis, decreased systolic and diastolic function, and decreased left ventricular remodeling. Transiently or stably overexpression of mitochondria Omi/HtrA2 in H9C2 cells enhance apoptosis as evidenced by elevated caspase-3, -9 activity and TUNEL staining, which was completely blocked by Ucf-101, a specific Omi/HtrA2 inhibitor. Mechanistic studies revealed mitochondrial Omi/HtrA2 overexpression degraded the mitochondrial anti-apoptotic protein HAX-1, an effect attenuated by Ucf-101. Additionally, transfected cells overexpressing mitochondrial Omi/HtrA2 were more sensitive to hypoxia and reoxygenation (H/R) induced apoptosis. Cyclosporine A (CsA), a mitochondrial permeability transition inhibitor, blocked translocation of Omi/HtrA2 from mitochondrial to cytoplasm, and protected transfected cells incompletely against H/R-induced caspase-3 activation. We report in vitro and in vivo overexpression of mitochondrial Omi/HtrA2 induces cardiac apoptosis and dysfunction. Thus, strategies to directly inhibit Omi/HtrA2 or its cytosolic translocation from mitochondria may protect against heart injury.
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