期刊
JOURNAL OF PHYSIOLOGICAL SCIENCES
卷 67, 期 6, 页码 639-654出版社
SPRINGER JAPAN KK
DOI: 10.1007/s12576-017-0555-7
关键词
Endurance exercise; Autophagy; Mitophagy; Ischemia reperfusion; Heart
类别
资金
- University of West Florida though the Office of Research and Sponsored Programs [164336]
- UWF [CF6672, R0036]
Cardiac myocytes are terminally differentiated cells and possess extremely limited regenerative capacity; therefore, preservation of mature cardiac myocytes throughout the individual's entire life span contributes substantially to healthy living. Autophagy, a lysosome-dependent cellular catabolic process, is essential for normal cardiac function and mitochondria maintenance. Therefore, it may be reasonable to hypothesize that if endurance exercise promotes cardiac autophagy and mitochondrial autophagy or mitophagy, exercise-induced cardiac autophagy (EICA) or exercise-induced cardiac mitophagy (EICM) may confer propitious cellular environment and thus protect the heart against detrimental stresses, such as an ischemia-reperfusion (I/R) injury. However, although the body of evidence supporting EICA and EICM is growing, the molecular mechanisms of EICA and EICM and their possible roles in cardioprotection against an I/R injury are poorly understood. Here, we introduce the general mechanisms of autophagy in an attempt to integrate potential molecular pathways of EICA and EICM and also highlight a potential insight into EICA and EICM in cardioprotection against an I/R insult.
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