ArticleJournal of diabetes and metabolic disorders2014
Inhibition of mitochondrial permeability transition pore restores the cardioprotection by postconditioning in diabetic hearts.
Article in Journal of diabetes and metabolic disorders, 2014. 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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Who cites it
16 citing papers in PubMed, 36 citations in OpenAlex.
- Protective effect of ischaemic postconditioning combined with nicorandil on myocardial ischaemia‒reperfusion injury in diabetic rats.BMC cardiovascular disorders · 2022Article
- Experimental and molecular docking studies of quercetin and vitamin E with diabetes-associated mitochondrial-ATPase as anti-apoptotic therapeutic strategies.Journal of diabetes and metabolic disorders · 2022Article
- Alisporivir Normalizes Mitochondrial Function of Primary Mouse Lung Endothelial Cells Under Conditions of Hyperglycemia.Biochemistry. Biokhimiia · 2022Article
- Quercetin and vitamin E ameliorate cardio-apoptotic risks in diabetic rats.Molecular and cellular biochemistry · 2022Article
- Beyond the myocardium? SGLT2 inhibitors target peripheral components of reduced oxygen flux in the diabetic patient with heart failure with preserved ejection fraction.Heart failure reviews · 2022Review
- Terpene-rich fractions of Ficus mucoso (Welw) modulate lipopolysaccharide-induced inflammatory mediators and aberrant permeability of the inner mitochondrial membrane in murine animal model.Inflammopharmacology · 2021Article
- Alisporivir Treatment Alleviates Mitochondrial Dysfunction in the Skeletal Muscles of C57BL/6NCrl Mice with High-Fat Diet/Streptozotocin-Induced Diabetes Mellitus.International journal of molecular sciences · 2021Article
- Article
- Diabetes Mellitus, Mitochondrial Dysfunction and CaInternational journal of molecular sciences · 2020Review
- Effects of troxerutin on vascular inflammatory mediators and expression of microRNA-146a/NF-κB signaling pathway in aorta of healthy and diabetic rats.The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology · 2020Article
- Hydrogen sulfide inhibits CaAmerican journal of physiology. Endocrinology and metabolism · 2019Article
- The application of remote ischemic conditioning in cardiac surgery.F1000Research · 2017Review
- Effect of ischemic postconditioning on myocardial protection in patients undergoing coronary artery bypass grafting surgery with cardiopulmonary bypass.Journal of cardiovascular and thoracic research · 2016Article
- Pharmacological Inhibition of NLRP3 Inflammasome Attenuates Myocardial Ischemia/Reperfusion Injury by Activation of RISK and Mitochondrial Pathways.Oxidative medicine and cellular longevity · 2016Article
- Experimental Diabetes Mellitus in Different Animal Models.Journal of diabetes research · 2016Review
- Contribution of apoptosis in myocardial reperfusion injury and loss of cardioprotection in diabetes mellitus.The journal of physiological sciences : JPS · 2015Review
Corrections and comments
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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
backgroundCardiovascular risk factors, including diabetes mellitus may attenuate the cardioprotection by postconditioning. This study aimed to investigate the cardioprotective effect of ischemic-postconditioning (IPostC) against ischemia/reperfusion injury in normal and chronically type-1 diabetic rats and the effect of mitochondrial permeability transition pore (mPTP) inhibition in this field.
methodsDiabetes was induced by a single intra-peritoneal injection of streptozotocin (50 mg/kg) in Wistar male rats (250-300 g). After 8 weeks, the hearts of control and diabetic animals were isolated and mounted on a constant-pressure Langendorff apparatus. All hearts were subjected to 30 min regional ischemia followed by 45 min reperfusion (by occluding and re-opening of LAD coronary artery, respectively). At the end of ischemia, the hearts received IPostC, cyclosporine-A, or both or none of them. Myocardial creatine-kinase (CK) release as an index of tissue injury was measured spectrophotometery in coronary effluent in reperfusion phase. Infarct size was identified by triphenyltetrazolium chloride staining. Heart rate, left ventricular end-diastolic pressure (LVEDP), LV systolic pressure (LVSP), rate-pressure product (RPP) and coronary flow were recorded throughout the experiment.
resultsIPostC, applied at the onset of reperfusion, failed to improve myocardial LVEDP and RPP, or reduce tissue damage indicated by infarct size and CK release in diabetic hearts, while it significantly recovered these parameters toward the pre-ischemic values in control hearts (P < 0.05). In contrast, with simultaneous inhibition of mPTP using cyclosporine-A, the cardioprotective effects of IPostC on myocardial hemodynamics, infarct size and CK release were significantly restored in diabetic hearts (P < 0.05).
conclusionsThe loss of cardioprotection by IPostC in diabetic state can be overcome by increasing the potency of protective IPostC through its co-application with mPTP inhibition.
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