Heat and mitochondrial bioenergetics

IF 2.5 Q2 PHYSIOLOGY
Alex T Von Schulze , Paige C Geiger
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引用次数: 2

Abstract

Recurrent heat treatment (HT) is known to improve mitochondrial respiratory function and reduce mitochondrial reactive oxygen species (mROS) production over time. Counterintuitively, HT results in acute mitochondrial stress characterized by impaired mitochondrial respiratory function and increased mROS production. The combination of reduced adenosine triphosphate (ATP) synthesis and elevated mROS production leads to the activation of the adenosine monophosphate (AMP)-activated protein kinase, nuclear factor erythroid-2-related factor 2, proliferator-activated receptor gamma coactivator 1-alpha, and nuclear respiratory factor-1 signaling cascades, as well as the heat-shock response via activation of heat-shock factor 1. The coordinated transcriptional control of these proteins leads to the chronological induction of mitochondrial quality-control mechanisms, such as mitophagy and chaperone-mediated autophagy, and mitochondrial biogenesis/remodeling. Taken together, the acute stress imposed by HT leads to positive adaptations in mitochondrial health and function over time — making HT an attractive, nonpharmacologic treatment option for conditions characterized by mitochondrial dysfunction.

热与线粒体生物能量学
随着时间的推移,反复热处理(HT)可以改善线粒体呼吸功能,减少线粒体活性氧(mROS)的产生。与直觉相反,高温会导致急性线粒体应激,其特征是线粒体呼吸功能受损和mROS产生增加。三磷酸腺苷(ATP)合成减少和mROS生成升高的结合导致单磷酸腺苷(AMP)激活的蛋白激酶、核因子红细胞2相关因子2、增殖因子激活受体γ辅激活因子1- α和核呼吸因子-1信号级联的激活,以及通过热休克因子1的激活而产生的热休克反应。这些蛋白的协调转录控制导致线粒体质量控制机制的时序诱导,如线粒体自噬和伴侣介导的自噬,以及线粒体的生物发生/重塑。总之,HT造成的急性应激导致线粒体健康和功能随时间的积极适应,使HT成为线粒体功能障碍的有吸引力的非药物治疗选择。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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来源期刊
Current Opinion in Physiology
Current Opinion in Physiology Medicine-Physiology (medical)
CiteScore
5.80
自引率
0.00%
发文量
52
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