:
There is considerable evidence in the heart 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). Aside from 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 this review is 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.
Transition mutation in codon 248 of the p53 tumor suppressor gene induced by reactive oxygen species and a nitric oxide-releasing compound
