Mitochondrial effectors of cellular senescence: beyond the free radical theory of aging

Aging Cell

Dorian V. Ziegler²  Christopher D. Wiley¹ 

[1] Buck Institute for Research on Aging, Novato, CA, USA;Département de Biologie, Ecole Normale Supérieure de Lyon, Lyon, France

关键词: aging;    bioenergetics;    cellular senescence;    electron transport chain;    metabolism;    mitochondria;    NAD;    reactive oxygen species;   

DOI  :  10.1111/acel.12287

来源: Wiley

【 摘 要 】

Summary

Cellular senescence is a process that results from a variety of stresses, leading to a state of irreversible growth arrest. Senescent cells accumulate during aging and have been implicated in promoting a variety of age-related diseases. Mitochondrial stress is an effective inducer of cellular senescence, but the mechanisms by which mitochondria regulate permanent cell growth arrest are largely unexplored. Here, we review some of the mitochondrial signaling pathways that participate in establishing cellular senescence. We discuss the role of mitochondrial reactive oxygen species (ROS), mitochondrial dynamics (fission and fusion), the electron transport chain (ETC), bioenergetic balance, redox state, metabolic signature, and calcium homeostasis in controlling cellular growth arrest. We emphasize that multiple mitochondrial signaling pathways, besides mitochondrial ROS, can induce cellular senescence. Together, these pathways provide a broader perspective for studying the contribution of mitochondrial stress to aging, linking mitochondrial dysfunction and aging through the process of cellular senescence.

【 授权许可】

CC BY   
© 2014 The Authors. Aging Cell published by the Anatomical Society and John Wiley & Sons Ltd.

Creative Commons Attribution License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited.