Autophagy, dysglycemia and myocardial infarction

Abstract

Autophagy has been thought as a novel cell death mechanism involving in the pathophysiological process of myocardial infarction (MI), and modulation of autophagy may be considered as a promising treatment modality for MI. Dysglycemia was associated with higher mortality in patients with MI. We hypothesize that autophagy may be a potential pathway through which dysglycemia has an impact on the outcomes of MI. In this review, we summarize the function of autophagy in the conditions of MI and the regulatory effects of dysglycemia on autophagy. Four main impacts of autophagy on MI under dysglycemia have been revealed. The first one is that autophagy limits the infarct size via inhibited mTOR. The second one is that autophagy promotes the survival of cardiomyocytes through depleted ATP. The third one is that autophagy protects cardiac myocytes from imparing by way of degradation. The last one is that autophagy maintenance of LV function through FoxO1. Therefore, the ability to modulate autophagy may represent as a potential and promising therapeutic strategy in limiting MI caused by dysglycemia. However, elucidation of precise ways of autophagy in mediating MI caused by dysglycemia, as well as when and how autophagy is manipulated remains us to research.