The Importance of Restoring the Adiponectin Signaling Pathway to Reduce Myocardial Reperfusion Injury in Diabetes.

Abstract

The incidence of heart failure after an acute myocardial infarction (AMI) remains unacceptably high despite medical advances in the past several years (1). Therefore, the discovery of new drugs or strategies to reduce myocardial damage in patients with AMI is urgently warranted. This problem is exacerbated particularly in those affected by diabetes. Diabetes significantly reduces myocardial ischemic tolerance after a sudden coronary artery occlusion, thereby leading to increased ischemic and reperfusion (IR) injuries (2). During the past several years, ischemic postconditioning (IPo) has emerged as an efficient intervention to reduce reperfusion injury and infarct size in patients with AMI (3). It consists of very short repetitive episodes of IR applied at the immediate onset of reperfusion after a prolonged coronary artery occlusion. Unfortunately, previous experimental studies demonstrated that the beneficial effects of IPo are largely lost in the presence of diabetes, although the mechanisms underlying this phenomenon remain to be fully clarified (2). In their study in this issue of Diabetes , Li et al. (4) demonstrate that type 1 diabetes abrogates the beneficial effects of IPo through the disruption of adiponectin signaling. Adiponectin is an adipocytokine that regulates glucose and fatty acid metabolism, exerting antioxidant, anti-inflammatory, and pro-survival effects (5). Adiponectin is also synthetized and secreted by cardiomyocytes, protecting against myocardial IR injury (5,6). Li et al. demonstrate …