Exercise-induced mitophagy in skeletal muscle occurs in the absence of stabilization of Pink1 on mitochondria
Exercise-induced mitophagy in skeletal muscle occurs in the absence of stabilization of Pink1 on mitochondria
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DOI：
10.1080/15384101.2018.1559556
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发表时间：
2019-01-02
期刊：
影响因子：
4.3
通讯作者：
Yan, Zhen
中科院分区：
文献类型：
--
作者：
Drake, Joshua C.;Laker, Rhianna C.;Yan, Zhen
线粒体质量的维持对骨骼肌功能和整体健康至关重要。运动训练激发线粒体的深刻适应，以改善骨骼肌线粒体的质量。我们最近已经证明，急性运动通过Ampk-Ulk 1信号级联反应促进骨骼肌中线粒体自噬清除受损/功能障碍的线粒体。在这个额外的视图中，我们探索Pink 1是否在运动后稳定在线粒体上作为线粒体自噬的信号。我们观察到没有可辨别的存在Pink 1从骨骼肌中分离的线粒体在任何时间点急性运动后，相反，明确的证据表明，稳定的Pink 1在HeLa细胞的线粒体与解偶联剂羰基氰间氯苯腙（CCCP）治疗后。综上所述，我们得出结论，Pink 1不参与运动诱导的骨骼肌线粒体自噬。
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.