期刊
CELL CYCLE
卷 18, 期 1, 页码 1-6出版社
TAYLOR & FRANCIS INC
DOI: 10.1080/15384101.2018.1559556
关键词
Mitophagy; skeletal muscle; exercise; Pink1
类别
资金
- National Institutes of Health [R01-AR050429, K99-AG057825, T32 HL007284-37]
- American Diabetes Association [1-16-PDF-030]
- American Heart Association [14POST20450061, 114PRE20380254]
- National Institute of Arthritis and Musculoskeletal and Skin Diseases [R01-AR050429]
- National Institute on Aging [K99-AG057825]
Maintenance of mitochondrial quality is essential for skeletal muscle function and overall health. Exercise training elicits profound adaptations to mitochondria to improve mitochondrial quality in skeletal muscle. We have recently demonstrated that acute exercise promotes removal of damaged/dysfunctional mitochondria via mitophagy in skeletal muscle during recovery through the Ampk-Ulk1 signaling cascade. In this Extra View, we explore whether Pink1 is stabilized on mitochondria following exercise as the signal for mitophagy. We observed no discernable presence of Pink1 in isolated mitochondria from skeletal muscle at any time point following acute exercise, in contrast to clear evidence of stabilization of Pink1 on mitochondria in HeLa cells following treatment with the uncoupler carbonyl cyanide m-chlorophenyl hydrazone (CCCP). Taken together, we conclude that Pink1 is not involved in exercise-induced mitophagy in skeletal muscle.
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据