期刊
ANNUAL REVIEW OF PHYSIOLOGY
卷 72, 期 -, 页码 45-59出版社
ANNUAL REVIEWS
DOI: 10.1146/annurev-physiol-021909-135757
关键词
autophagosome; autophagy; bafilomycin A1; calcium overload; cardioprotection; catabolism/anabolism balance; chloroquine; exosome; flux; frustrated autophagy; glutathione; ischemia/reperfusion; ischemic preconditioning; lysosome; mitochondria; mitochondrial quality control; mitophagy; phagophore; preconditioning
类别
资金
- NIH [R01 AG33283, P01 HL85577, R01 HL34579]
- NATIONAL HEART, LUNG, AND BLOOD INSTITUTE [P01HL085577, R01HL034579] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE ON AGING [R01AG033283] Funding Source: NIH RePORTER
The study of autophagy has been transformed by the cloning of most genes in the pathway and the introduction of GFP-LC3 as a reporter to allow visual assessment of autophagy. The field of cardiac biology is not alone in attempting to understand the implications of autophagy. The purpose of this review is to address some of the controversies and conundrums associated with the evolving studies of autophagy in the heart. Autophagy is a cellular process involving a complex orchestration of regulatory gene products as well as machinery for assembly, selective targeting, and degradation of autophagosomes and their contents. Our understanding of the role of autophagy in human disease is rapidly evolving as investigators examine the process in different tissues and different pathophysiological contexts. In the field of heart disease, autophagy has been examined in the settings of ischemia and reperfusion, preconditioning, cardiac hypertrophy, and heart failure. This review addresses the role of autophagy in cardioprotection, the balance of catabolism and anabolism, the concept of mitochondrial quality control, and the implications of impaired autophagic flux or frustrated autophagy.
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