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The Role of Autophagy During Myocardial Ischemia/Reperfusion Injury
Author(s) -
Ibe Al C.,
McIntyre Anahi,
Kim Alissa,
Kim Hannah,
Castellano Andrew,
Young Lindon,
Barsotti Robert,
Chen Qian
Publication year - 2018
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.2018.32.1_supplement.717.21
Subject(s) - autophagy , ischemia , medicine , reperfusion injury , trehalose , cardiology , endocrinology , pharmacology , apoptosis , chemistry , biochemistry
Autophagy is a housekeeping process to degrade protein aggregates, damaged cytoplasmic constituents, and provides adaptation when cells go through a nutrient stress. However, a debate persists on whether autophagy is beneficial to attenuate or promote cell damage under an ischemia/reperfusion (I/R) insult to the heart. This study tested the effects of an autophagy enhancer (e.g. rapamycin and trehalose) on heart function and infarct size after global ischemia (30 min)/reperfusion (45 min) when given prior to ischemia (pretreatment) or at the beginning of reperfusion (posttreatment). We found that rapamycin pretreatment (25 nM, n=5) significantly restored left ventricular developed pressure (LVDP) to 64±5 % of initial baseline compared to control I/R hearts (n=8) which only recovered to 31±10% of initial baseline (p<0.01). Likewise, trehalose pretreatment (5 mM, n=7) and posttreatment (5 mM, n=6) significantly restored final LVDP to 62±5% and 65±4% of initial baseline, respectively compared to control I/R hearts (both p<0.01). Moreover, infarction percentage after I/R is significantly reduced in rapamycin post‐treated hearts (23±4%, p<0.05) and trehalose treated hearts (20±4% for pretreatment and 15±3% for posttreatment, both p<0.01) when compared to control I/R hearts (41±4%). The preliminary data suggest that autophagy enhancement before ischemia or at reperfusion may be beneficial for reducing I/R injury This study was supported by the Center for Chronic Disorders of Aging, the Division of Research and the Department of Bio‐Medical Sciences at Philadelphia College of Osteopathic Medicine. This abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal .