Coenzyme Q redox signalling and longevity
Coenzyme Q redox signalling and longevity
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DOI：
10.1016/j.freeradbiomed.2021.01.018
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发表时间：
2021-01-18
影响因子：
7.4
通讯作者：
Sanz, Alberto
中科院分区：
文献类型：
--
作者：
Scialo, Filippo;Sanz, Alberto
线粒体是细胞的动力源。它们产生了我们生长、生存和繁殖所需的大量能量。以三磷酸腺苷的形式产生能量的同一系统也产生活性氧物种(ROS)。线粒体活性氧(MtROS)多年来一直被认为是代谢的有毒副产物，与衰老和许多退行性疾病有关。今天，我们知道mtROS是决定细胞命运和维持细胞动态平衡所必需的基本氧化还原信使。大多数线粒体ROS是由呼吸复合体I(CI)和复合体III(CIII)产生的。CI和CIII产生ROS的方式和时间取决于辅酶Q(CoQ)池的氧化还原状态和呼吸过程中产生的质子动力(PMF)。在衰老过程中，有缺陷的线粒体积累，从而产生高水平的mtROS。这会导致氧化应激，并扰乱氧化还原信号。在这里，我们回顾了mtROS是如何在年轻和老年线粒体中产生的，以及CI和CIII衍生的ROS如何控制生理和病理过程。最后，我们讨论了为什么损伤的线粒体在衰老过程中积累，以及随着年龄的增长保存线粒体氧化还原信号的方法。
Mitochondria are the powerhouses of the cell. They produce a significant amount of the energy we need to grow, survive and reproduce. The same system that generates energy in the form of ATP also produces Reactive Oxygen Species (ROS). Mitochondrial Reactive Oxygen Species (mtROS) were considered for many years toxic byproducts of metabolism, responsible for ageing and many degenerative diseases. Today, we know that mtROS are essential redox messengers required to determine cell fate and maintain cellular homeostasis. Most mtROS are produced by respiratory complex I (CI) and complex III (CIII). How and when CI and CIII produce ROS is determined by the redox state of the Coenzyme Q (CoQ) pool and the proton motive force (pmf) generated during respiration. During ageing, there is an accumulation of defective mitochondria that generate high levels of mtROS. This causes oxidative stress and disrupts redox signalling. Here, we review how mtROS are generated in young and old mitochondria and how CI and CIII derived ROS control physiological and pathological processes. Finally, we discuss why damaged mitochondria amass during ageing as well as methods to preserve mitochondrial redox signalling with age.