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细胞衰老将线粒体-内质网接触点与衰老联系起来。

Cellular senescence links mitochondria-ER contacts and aging.

机构信息

Centre de Recherche en Cancérologie de Lyon, Inserm U1052, CNRS UMR 5286, Université de Lyon, Centre Léon Bérard, Lyon, France.

Center for Integrative Genomics, University of Lausanne, Lausanne, Switzerland.

出版信息

Commun Biol. 2021 Nov 24;4(1):1323. doi: 10.1038/s42003-021-02840-5.

DOI:10.1038/s42003-021-02840-5
PMID:34819602
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8613202/
Abstract

Membrane contact sites emerged in the last decade as key players in the integration, regulation and transmission of many signals within cells, with critical impact in multiple pathophysiological contexts. Numerous studies accordingly point to a role for mitochondria-endoplasmic reticulum contacts (MERCs) in modulating aging. Nonetheless, the driving cellular mechanisms behind this role remain unclear. Recent evidence unravelled that MERCs regulate cellular senescence, a state of permanent proliferation arrest associated with a pro-inflammatory secretome, which could mediate MERC impact on aging. Here we discuss this idea in light of recent advances supporting an interplay between MERCs, cellular senescence and aging.

摘要

膜接触位点在过去十年中作为细胞内许多信号整合、调节和传递的关键参与者出现,对多种病理生理情况下都有重要影响。因此,许多研究表明线粒体-内质网接触(MERCs)在调节衰老方面发挥作用。然而,这种作用背后的驱动细胞机制尚不清楚。最近的证据揭示了 MERCs 调节细胞衰老,这是一种与促炎分泌组相关的永久性增殖停滞状态,这可能介导了 MERC 对衰老的影响。本文我们根据支持 MERCs、细胞衰老和衰老之间相互作用的最新进展来讨论这一观点。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2e42/8613202/27ae9f1abbe2/42003_2021_2840_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2e42/8613202/734caf169c85/42003_2021_2840_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2e42/8613202/12932aa1a256/42003_2021_2840_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2e42/8613202/27ae9f1abbe2/42003_2021_2840_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2e42/8613202/734caf169c85/42003_2021_2840_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2e42/8613202/12932aa1a256/42003_2021_2840_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2e42/8613202/27ae9f1abbe2/42003_2021_2840_Fig3_HTML.jpg

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BAP31: Physiological functions and roles in disease.BAP31:生理功能与疾病中的作用。
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Noncanonical function of Pannexin1 promotes cellular senescence and renal fibrosis post-acute kidney injury.Pannexin1的非经典功能促进急性肾损伤后细胞衰老和肾纤维化。
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Alcohol, Anti-HIV Drugs, and/or Hippuric Acid Deteriorate Cellular Stresses in Senescent Hepatocytes and Aging Murine Liver.酒精、抗HIV药物和/或马尿酸会加剧衰老肝细胞和衰老小鼠肝脏中的细胞应激。
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