Adiponectin

Abstract

Key Words: diabetes Ⅲ myocardial infarction Ⅲ adipocytokine Ⅲ signaling D iabetes mellitus and its resultant cardiovascular disease are a dominant public health problem. The hyperglycemia and hyperlipidemia associated with diabetes mellitus not only result in vascular injury causing greater myocardial infarction (MI) morbidity but also directly impact ischemic cardiomyocytes adversely, causing larger infarct size 1,2 and more severe heart failure 3 after MI, further contributing to higher mortality. Effective therapeutic interventions enhancing tissue insulin sensitivity and improving cellular metabolism may therefore not only attenuate diabetic injury, but also reduce the risk of MI and death of cardiovascular etiology.Peroxisome proliferator-activated receptors (PPARs) (including PPAR␣, -␦ and, -␥) are transcription factors belonging to the nuclear receptor super family. 4 PPAR␥ agonists such as rosiglitazone (RSG) and pioglitazone are insulin sensitizers and have been used widely in the treatment of type 2 diabetes. Numerous experimental studies have demonstrated that PPAR␥ agonist treatment not only attenuates vascular injury in diabetic animals, 5-7 thus reducing the incidence of MI, but also exerts direct protective effect on ischemic cardiomyocytes 8,9 and improves post-MI cardiac function recovery. Moreover, several clinical studies, 10 -12 including one recently published, 13 have demonstrated that RSG treatment reduces coronary events following percutaneous coronary intervention and retards atherosclerosis disease progression. However, 2 metaanalyses 14,15 reported that longterm treatment of advanced diabetic patients with RSG was associated with a significantly increased risk of MI and death Original

Role of Adipokines in Cardiovascular Disease

“…46 Interestingly, CTRP9 forms heterotrimers with APN, and appears to share the AdipoR1 in both cultured endothelial cells and cardio- ide production, culminating in unfavorable cardiovascular outcomes. 80 In a recent study investigating the direct mechanisms underlying both APN signaling and APN resistance, GRK2 phosphorylated APN receptor 1 post-MI impaired the cardioprotective functions of APN. 81 Inhibition of GRK2-mediated AdipoR1 phosphorylation represents a completely novel manner of restoring APN cardioprotective signaling in the post-MI injury period.…”

Fenofibrate promotes ischemia-induced revascularization through the adiponectin-dependent pathway

“…Clinically, circulating adiponectin levels are reduced in patients with obesity-linked complications, including type 2 diabetes and peripheral arterial occlusive disease (12,13,24). Thus, therapeutic approaches aimed at increasing adiponectin could be useful for treatment of cardiovascular disease (18,38).…”

Physiologic Remote Ischemic Training Offers a Cardioprotective Effect against Myocardial Infarction in a Time-Dependent Manner

“…Infarct sizes in PRIT subgroups were significant smaller than those in the control MI subgroups, and this post-MI reduction in infarct size was time dependent (Figure 4). Sudden occlusion of a major coronary artery can result in AMI and rapid apoptosis of cardiomyocytes, leading to progressive fibrous replacement in the myocardium and LV dilatation [3,25]. Previous studies [26][27][28] demonstrated that physiologic RIT could promote coronary collateral formation in the ischemic myocardium.…”