IMR Press / FBE / Volume 2 / Issue 3 / DOI: 10.2741/E174

Frontiers in Bioscience-Elite (FBE) is published by IMR Press from Volume 13 Issue 2 (2021). Previous articles were published by another publisher on a subscription basis, and they are hosted by IMR Press on imrpress.com as a courtesy and upon agreement with Frontiers in Bioscience.

Open Access Article
Role of autophagy in myocardial reperfusion injury
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1 Department of Physiology, Yanbian University, Yanji, China
2 Heart Institute, North China Coal Medical University, Tangshan, China
3 Department of Anesthesiology, the University of North Carolina at Chapel Hill, NC 27599
Front. Biosci. (Elite Ed) 2010, 2(3), 1147–1153; https://doi.org/10.2741/E174
Published: 1 June 2010
Abstract

While autophagy is induced by myocardial ischemia/reperfusion, it is unclear whether autophagy is detrimental or beneficial to myocardial survival during ischemia/reperfusion. Isolated rat hearts were subjected to 30 min regional ischemia followed by 2 h of reperfusion. Autophagy was determined by the ratio of LC3 -II to LC3-I with Western blotting. Autophagy was prominent upon reperfusion but not during ischemia in rat hearts, indicating that autophagy may play a role during reperfusion phase. Ischemia or reperfusion did not enhance Beclin 1 expression, suggesting that Beclin 1 may not be critical for the formation of autophagy in isolated rat hearts. 3-methyladenine (3-MA), a classical inhibitor of autophagy, suppressed reperfusion-induced autophagy and reduced the infarct size when introduced at reperfusion. NECA, an agonist of adenosine receptors, and morphine also reduced the formation of autophagy as well as the infarct size when introduced at reperfusion. These data suggest that autophagy may play a detrimental role during reperfusion and that modulation of autophagy may prevent reperfusion injury in rat hearts. 

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