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The role and modulation of autophagy in experimental models of myocardial ischemia-reperfusion injury

Published on Dec 1, 2014in Journal of Geriatric Cardiology1.76
· DOI :10.11909/j.issn.1671-5411.2014.01.009
Carol Chen-Scarabelli15
Estimated H-index: 15
,
Pratik R. Agrawal4
Estimated H-index: 4
+ 7 AuthorsRichard A. Knight47
Estimated H-index: 47
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Abstract
A physiological sequence called autophagy qualitatively determines cellular viability by removing protein aggregates and damaged cytoplasmic constituents, and contributes significantly to the degree of myocardial ischemia-reperfusion (I/R) injury. This tightly orchestrated catabolic cellular ‘housekeeping’ process provides cells with a new source of energy to adapt to stressful conditions. This process was first described as a pro-survival mechanism, but increasing evidence suggests that it can also lead to the demise of the cell. Autophagy has been implicated in the pathogenesis of multiple cardiac conditions including myocardial I/R injury. However, a debate persists as to whether autophagy acts as a protective mechanism or contributes to the injurious effects of I/R injury in the heart. This controversy may stem from several factors including the variability in the experimental models and species, and the methodology used to assess autophagy. This review provides updated knowledge on the modulation and role of autophagy in isolated cardiac cells subjected to I/R, and the growing interest towards manipulating autophagy to increase the survival of cardiac myocytes under conditions of stress-most notably being I/R injury. Perturbation of this evolutionarily conserved intracellular cleansing autophagy mechanism, by targeted modulation through, among others, mammalian target of rapamycin (mTOR) inhibitors, adenosine monophosphate-activated protein kinase (AMPK) modulators, calcium lowering agents, resveratrol, longevinex, sirtuin activators, the proapoptotic gene Bnip3, IP3 and lysosome inhibitors, may confer resistance to heart cells against I/R induced cell death. Thus, therapeutic manipulation of autophagy in the challenged myocardium may benefit post-infarction cardiac healing and remodeling.
  • References (33)
  • Citations (24)
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References33
Newest
#1Jian Xiao ('SMMU': Second Military Medical University)H-Index: 9
#2Xiaoyan Zhu ('SMMU': Second Military Medical University)H-Index: 1
Last.Xin Ni ('SMMU': Second Military Medical University)H-Index: 1
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#1Narasimman Gurusamy (UConn: University of Connecticut)H-Index: 27
#2Istvan Lekli (UConn: University of Connecticut)H-Index: 23
Last.Dipak K. Das (UConn: University of Connecticut)H-Index: 81
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#1Narasimman Gurusamy (UConn: University of Connecticut)H-Index: 27
#2Istvan Lekli (UConn: University of Connecticut)H-Index: 23
Last.Dipak K. Das (UConn: University of Connecticut)H-Index: 81
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#2Hailong Han (CSU: Central South University)H-Index: 3
Last.Zhuohua Zhang (CSU: Central South University)H-Index: 12
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#1Wei Cheng (Peking Union Medical College Hospital)H-Index: 1
#2Wei Cheng Mm (Peking Union Medical College Hospital)
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#1Mingming Sun (UW: University of Wyoming)H-Index: 1
#2Ying Tan (UW: University of Wyoming)
Last.Wei Guo (UW: University of Wyoming)H-Index: 8
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#1Jing Wang (Nanjing University of Chinese Medicine)H-Index: 1
#2Meng-Ling Wu (Nanjing University of Chinese Medicine)H-Index: 1
Last.Yao-Hong Song (Nanjing University of Chinese Medicine)H-Index: 1
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#1Jun Ren (Fudan University)H-Index: 57
#2James R. Sowers (MU: University of Missouri)H-Index: 83
Last.Yingmei Zhang (Fudan University)H-Index: 1
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