ArticleAge (Dordrecht, Netherlands)2013
Variations in the protein level of Omi/HtrA2 in the heart of aged rats may contribute to the increased susceptibility of cardiomyocytes to ischemia/reperfusion injury and cell death : Omi/HtrA2 and aged heart injury.
Article in Age (Dordrecht, Netherlands), 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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16 citing papers in PubMed, 40 citations in OpenAlex.
- Phytoestrogen α-Zearalanol attenuates homocysteine-induced apoptosis in human umbilical vein endothelial cells.BioMed research international · 2013Trial
- Ucf-101 alleviates Ischaemia/Reperfusion induced retinal inflammation and injury via suppressing oxidative damage.Journal of molecular histology · 2024Article
- Effects of resveratrol on tolerance to ischemia/reperfusion injury in aged male mice: Role of autophagy and apoptosis.Food science & nutrition · 2023Article
- 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
- Extracellular HtrA2 Induces Apoptosis in Human Umbilical Vein Endothelial Cells.International journal of molecular sciences · 2019Article
- Article
- The protective effects of ischemic preconditioning on rats with renal ischemia-reperfusion injury and the effects on the expression of Bcl-2 and Bax.Experimental and therapeutic medicine · 2017Article
- Responses of A549 human lung epithelial cells to cristobalite and α-quartz exposures assessed by toxicoproteomics and gene expression analysis.Journal of applied toxicology : JAT · 2017Article
- Cardiac Specific Overexpression of Mitochondrial Omi/HtrA2 Induces Myocardial Apoptosis and Cardiac Dysfunction.Scientific reports · 2016Article
- Ischemia/Reperfusion.Comprehensive Physiology · 2016Review
- Mitochondrial Metabolism in Aging Heart.Circulation research · 2016Review
- Cloning and Transcriptional Activity of the Mouse Omi/HtrA2 Gene Promoter.International journal of molecular sciences · 2016Article
- Mitochondrial quality control in the myocardium: cooperation between protein degradation and mitophagy.Journal of molecular and cellular cardiology · 2014Review
- Thioredoxin reductase was nitrated in the aging heart after myocardial ischemia/reperfusion.Rejuvenation research · 2013Article
- Alleviation of hyperglycemia induced vascular endothelial injury by exenatide might be related to the reduction of nitrooxidative stress.BioMed research international · 2013Article
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Authors and funding
10 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Survival after acute myocardial infarction is decreased in elderly patients. The enhanced rates of apoptosis in the aging heart exacerbate myocardial ischemia/reperfusion (MI/R) injury. We have recently demonstrated that the X-linked inhibitor of apoptosis protein (XIAP), the most potent endogenous inhibitor of apoptosis, was decreased in aging rats' hearts. XIAP was balanced by two mitochondria proteins, Omi/HtrA2 and Smac/DIABLO. However, the implicative role of XIAP, Omi/HtrA2, and Smac/DIABLO to aging-related MI/R injury has not been previously investigated. In our study, male aging rats (20-24 months) or young adult rats (4-6 months) were subjected to 30 min of myocardial ischemia followed by reperfusion. MI/R-induced cardiac injury was enhanced in aging rats, as evidenced by aggravated cardiac dysfunction, enlarged infarct size, and increased myocardial apoptosis (TUNEL and caspase-3 activity). Then, the XIAP, Omi/HtrA2, and Smac/DIABLO protein and mRNA expression was detected. XIAP protein and mRNA expression was decreased in both aging hearts and aging hearts subjected to MI/R. Meanwhile, myocardial XIAP protein expression was correlated to cardiac function after MI/R. However, Omi/HtrA2, but not Smac/DIABLO, expression was increased in aging hearts. Moreover, the translocation of Omi/HtrA2 from mitochondria to cytosol was increased in both aging hearts and aging hearts subjected to MI/R. Treatment with ucf-101 (a novel and specific Omi/HtrA2 inhibitor) attenuated XIAP degradation and caspase-3 activity and exerted cardioprotective effects. Taken together, these results demonstrated that increased expression and leakage of Omi/HtrA2 enhanced MI/R injury in aging hearts via degrading XIAP and promoting myocardial apoptosis.
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