Abstract
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.
Keywords: Autophagy, heart, ischemia, reperfusion, kinases, H2S, nitric oxide.
Graphical Abstract
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