Submit Manuscript  

Article Details


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

Author(s):

Andrey Krylatov, Leonid Maslov*, Sergey Y. Tsibulnikov, Nikita Voronkov, Alla Boshchenko, James Downey and Robert Mentzer   Pages 1 - 9 ( 9 )

Abstract:


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.

Keywords:

Autophagy, heart, ischemia, reperfusion, kinases, H2S, nitric oxide.

Affiliation:

Cardiology Research Institute, Tomsk National Research Medical Center of the RAS, Tomsk, Cardiology Research Institute, Tomsk National Research Medical Center of the RAS, Tomsk, Cardiology Research Institute, Tomsk National Research Medical Center of the RAS, Tomsk, Cardiology Research Institute, Tomsk National Research Medical Center of the RAS, Tomsk, Cardiology Research Institute, Tomsk National Research Medical Center of the RAS, Tomsk, University of South Alabama College of Medicine, Mobile, Alabama, Molecular Cardiobiology, Smidt Heart Institute, CedarsSinai Medical Center, Los Angeles, California



Read Full-Text article