Trewin Adam J, Berry Brandon J, Wojtovich Andrew P
Departments of Anesthesiology and Perioperative Medicine, University of Rochester Medical Center; Rochester, NY 14642 , USA.
Pharmacology and Physiology, University of Rochester Medical Center, Rochester, NY 14642, USA.
Antioxidants (Basel). 2018 Jan 6;7(1):7. doi: 10.3390/antiox7010007.
Exercise is a robust stimulus for mitochondrial adaptations in skeletal muscle which consequently plays a central role in enhancing metabolic health. Despite this, the precise molecular events that underpin these beneficial effects remain elusive. In this review, we discuss molecular signals generated during exercise leading to altered mitochondrial morphology and dynamics. In particular, we focus on the interdependence between reactive oxygen species (ROS) and redox homeostasis, the sensing of cellular bioenergetic status via 5' adenosine monophosphate (AMP)-activated protein kinase (AMPK), and the regulation of mitochondrial fission and fusion. Precisely how exercise regulates the network of these responses and their effects on mitochondrial dynamics is not fully understood at present. We highlight the limitations that exist with the techniques currently available, and discuss novel molecular tools to potentially advance the fields of redox biology and mitochondrial bioenergetics. Ultimately, a greater understanding of these processes may lead to novel mitochondria-targeted therapeutic strategies to augment or mimic exercise in order to attenuate or reverse pathophysiology.
运动是骨骼肌线粒体适应性变化的一种强大刺激因素，因此在增强代谢健康方面起着核心作用。尽管如此，支撑这些有益作用的精确分子事件仍然难以捉摸。在这篇综述中，我们讨论了运动过程中产生的导致线粒体形态和动力学改变的分子信号。特别地，我们关注活性氧（ROS）与氧化还原稳态之间的相互依存关系、通过5'-腺苷单磷酸（AMP）激活的蛋白激酶（AMPK）对细胞生物能量状态的感知，以及线粒体分裂和融合的调控。目前尚不完全清楚运动究竟如何调节这些反应网络及其对线粒体动力学的影响。我们强调了现有技术存在的局限性，并讨论了可能推动氧化还原生物学和线粒体生物能量学领域发展的新型分子工具。最终，对这些过程的更深入理解可能会带来新的以线粒体为靶点的治疗策略，以增强或模拟运动，从而减轻或逆转病理生理学状态。
