Description

Abstract The AMP-activated protein kinase (AMPK) has been firstly discovered to be activated under metabolic stress conditions such as myocardial ischemia. Its protective action during an ischemic episode has been demonstrated by several research groups. By targeting metabolism, AMPK helps the heart to survive under such deleterious conditions. However, AMPK action extends beyond metabolism and acute stress conditions. Indeed, it has been more recently shown that AMPK acts as protector of the heart in several chronic diseases such heart failure, diabetic cardiomyopathy and cardiac hypertrophy by acting in cardiomyocytes but also on the other cell types such as fibroblasts. Very recently, our group discovered a connection between AMPK and a particular post-translational modification called O-GlcNAcylation, this interplay acting a major role in the development of cardiac hypertrophy. The lecture will focus on the different protective roles of cardiac AMPK.