The Role of Reactive Oxygen Species, Kinases, Hydrogen Sulfide, and Ni-tric Oxide in the Regulation of Autophagy and Their Impact on Ischemia and Reperfusion Injury in the Heart

There is considerable evidence that autophagy in cardiomyocytes is activated by hypoxia/reoxygenation (H/R) or in hearts by ischemia/reperfusion (I/R). Depending upon the experimental model and duration of ischemia, increases in autophagy in this setting maybe beneficial (cardioprotective) or deleterious (exacerbate I/R injury). Besides the conundrum as to whether or not autophagy is an adaptive process, it is clearly regulated by a number of diverse molecules, including reactive oxygen species (ROS), various kinases, hydrogen sulfide (H2S) and nitric oxide (NO). The purpose of this review was to address briefly the controversy regarding the role of autophagy in this setting and to examine a variety of disparate molecules that are involved in its regulation.

Automated summary

This text provides evidence that autophagy in cardiomyocytes can be activated by hypoxia/reoxygenation or ischemia/reperfusion, and discusses how increases in autophagy may have both beneficial and detrimental effects on the heart. It also highlights the regulation of autophagy by various molecules in this setting.