2022
DOI: 10.1007/s00018-022-04330-1
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Therapeutic potential of a single-dose melatonin in the attenuation of cardiac ischemia/reperfusion injury in prediabetic obese rats

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Cited by 9 publications
(3 citation statements)
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“…The contribution of melatonin in maintaining mitochondrial redox homeostasis by influencing the tricarboxylic acid cycle, mitochondrial oxidative phosphorylation, SIRT3, and SOD2 has recently been revealed [32]. Consistent with our findings, a recent study has shown the therapeutic potential of single-dose melatonin in the attenuation of cardiac IR injury in prediabetic obese rats through its ability to improve mitochondrial function and rebalance the mitochondrial dynamics [20].…”
Section: Discussionsupporting
confidence: 90%
See 1 more Smart Citation
“…The contribution of melatonin in maintaining mitochondrial redox homeostasis by influencing the tricarboxylic acid cycle, mitochondrial oxidative phosphorylation, SIRT3, and SOD2 has recently been revealed [32]. Consistent with our findings, a recent study has shown the therapeutic potential of single-dose melatonin in the attenuation of cardiac IR injury in prediabetic obese rats through its ability to improve mitochondrial function and rebalance the mitochondrial dynamics [20].…”
Section: Discussionsupporting
confidence: 90%
“…Melatonin increases the efficiency of mitochondrial oxidative phosphorylation and reduces electron leakage, thereby lowering free radical generation [15]. Interestingly, recent studies have shown that treatment with melatonin reduced mitochondrial dysfunction caused by cardiac ischemia-reperfusion injury in type 1 diabetic rats [19] as well as prediabetic obese rats [20].…”
Section: Introductionmentioning
confidence: 99%
“…Antioxidant effects were reported in Sprague–Dawley rats with myocardial ischemia/reperfusion injury, where MT decreased cardiac malondialdehyde while increasing cardiac SOD and GPx by activating the JAK2/STAT3 signaling pathway [ 134 ]. Similar results have been documented in other preclinical studies of cardiac ischemia/reperfusion injury [ 135 , 136 , 137 , 138 ]. Activation of cardiac MT2, but not MT1 receptors, may be responsible for this effect [ 139 ].…”
Section: Antioxidant Pharmacotherapies In Cardiorenal Diseasessupporting
confidence: 90%