Mitochondrial dysfunction in cell senescence and aging.
Mitochondrial dysfunction in cell senescence and aging.
复制标题
细胞衰老和老化中的线粒体功能障碍
DOI：
10.1172/jci158447
复制
发表时间：
2022-07-01
影响因子：
15.9
通讯作者：
von Zglinicki, Thomas
中科院分区：
文献类型：
--
作者：
Miwa, Satomi;Kashyap, Sonu;Chini, Eduardo;von Zglinicki, Thomas
线粒体功能障碍和细胞衰老是衰老的标志，并且密切相关。线粒体功能障碍，操作上定义为每单位线粒体呼吸能力降低以及线粒体膜电位降低，通常伴有氧自由基产生增加，是细胞衰老的原因和结果，并且在诱导和维持衰老表型的多个反馈回路中占突出地位。在这里，我们总结了导致衰老和老化中线粒体功能障碍的途径，并讨论了线粒体功能障碍的主要后果以及这些后果如何导致衰老和老化。我们还强调了衰老相关的线粒体功能障碍作为抗衰老和抗衰老干预目标的潜力，提出了多种干预措施的组合，将线粒体功能障碍作为新的，有效的衰老抑制剂。
Mitochondrial dysfunction and cell senescence are hallmarks of aging and are closely interconnected. Mitochondrial dysfunction, operationally defined as a decreased respiratory capacity per mitochondrion together with a decreased mitochondrial membrane potential, typically accompanied by increased production of oxygen free radicals, is a cause and a consequence of cellular senescence and figures prominently in multiple feedback loops that induce and maintain the senescent phenotype. Here, we summarize pathways that cause mitochondrial dysfunction in senescence and aging and discuss the major consequences of mitochondrial dysfunction and how these consequences contribute to senescence and aging. We also highlight the potential of senescence-associated mitochondrial dysfunction as an antiaging and antisenescence intervention target, proposing the combination of multiple interventions converging onto mitochondrial dysfunction as novel, potent senolytics.