ArticleOxidative medicine and cellular longevity2015
Genome-Wide Expression Profiling of Anoxia/Reoxygenation in Rat Cardiomyocytes Uncovers the Role of MitoKATP in Energy Homeostasis.
Article in Oxidative medicine and cellular longevity, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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10 citing papers in PubMed, 12 citations in OpenAlex.
- miR‑30c reduces myocardial ischemia/reperfusion injury by targeting SOX9 and suppressing pyroptosis.Experimental and therapeutic medicine · 2023Article
- Metabolomics analysis in rat hearts with ischemia/reperfusion injury after diazoxide postconditioning.Frontiers in molecular biosciences · 2023Article
- Mitochondrial proteomics alterations in rat hearts following ischemia/reperfusion and diazoxide post‑conditioning.Molecular medicine reports · 2021Article
- MicroRNA And Circular RNA Expression In Affected Skin Of Patients With Postherpetic Neuralgia.Journal of pain research · 2019Article
- Acyl-CoA dehydrogenase long chain expression is associated with esophageal squamous cell carcinoma progression and poor prognosis.OncoTargets and therapy · 2018Article
- miR-21 increases c-kitPeerJ · 2017Article
- Cytomembrane ATP-sensitive KExperimental and therapeutic medicine · 2016Article
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- miR-21 Reduces Hydrogen Peroxide-Induced Apoptosis in c-kitOxidative medicine and cellular longevity · 2016Article
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7 authors at 1 institution in 1 country.
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No grant is acknowledged in the PubMed record.
Abstract
Mitochondrial ATP-sensitive potassium channel (mitoK(ATP)) is a common end effector of many protective stimuli in myocardial ischemia-reperfusion injury (MIRI). However, the specific molecular mechanism underlying its myocardial protective effect is not well elucidated. We characterized an anoxia/reoxygenation (A/R) model using freshly isolated adult rat cardiomyocytes. MitoK(ATP) status was interfered with its specific opener diazoxide (DZ) or blocker 5-hydroxydecanote (5-HD). Digital gene expression (DGE) and bioinformatic analysis were deployed. Three energy metabolism related genes (MT-ND6, Idh2, and Acadl) were upregulated when mitoK(ATP) opened. In addition, as many as 20 differentially expressed genes (DEGs) were significantly enriched in five energy homeostasis correlated pathways (PPAR, TCA cycle, fatty acid metabolism, and peroxisome). These findings indicated that mitoK(ATP) opening in MIRI resulted in energy mobilization, which was confirmed by measuring ATP content in cardiomyocytes. These causal outcomes could be a molecular mechanism of myocardial protection of mitoKATP and suggested that the mitoK(ATP) opening plays a physiologic role in triggering cardiomyocytes' energy homeostasis during MIRI. Strategies of modulating energy expenditure during myocardial ischemia-reperfusion may be promising approaches to reduce MIRI.
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