Involvement of mitochondrial mechanisms in myocardial protection by ischemic postconditioning

Abstract

Background Myocardial ischemia/reperfusion injury (MI/RI) is life-threaten to the patients with cardiovascular diseases, and is a serious risk factor for the mortality of patients with diabetes mellitus. Ischemic postconditioning (IPO) effectively protects myocardia probably by strengthening the function of mitochondria. Objective To summarize mitochondrial mechanisms underlying myocardial protection after IPO. Content IPO protects myocardia probably by activating endogenous signal transduction pathways, involved in reperfusion injury salvage kinase(RISK) and survival activation factor enhancement(SAFE), followed by the release of endogenous trigger factors, such as adenosine. Adenosine can activate signal transduction and activator of transcription 3 (STAT3) and protein kinase C (PKC), then promote the phosphorylation of glycogen synthase kinase-3β (GSK-3β) , open mitochondrial sensitive potassium (mitoKATP) channel, and shut off mitochondrial permeability transition pores (mPTP) by increasing the expression of mitochondrial cardiolipin, connexin 43 (Cx43) and anti-apoptosis gene Bcl-2, thereafter remaining thioredoxin (Trx)2 and mitochondrial respiratory chain intact, and reduce MI/RI. Trend IPO protects myocardia in patients with diabetes mellitus by maintaining homeostasis of mitochondria. However, further investigations are needed to validate the proposed underlying mechanisms of myocardial protection by IPO, especially in diabetic MI/RI, and to confirm some specific signal transduction pathways as new therapeutic targets for MI/RI. Key words: Ischemia-reperfusion injury; Myocardial; Postconditioning; Mitochondria; Myocardial protection