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炎症和线粒体自噬是衰老的线粒体检查点。

Inflammation and mitophagy are mitochondrial checkpoints to aging.

机构信息

Department of Radiation Oncology, Weill Cornell Medicine, New York, NY, USA.

John B. Little Center for Radiation Sciences, Harvard T.H. Chan School of Public Health, Boston, MA, USA.

出版信息

Nat Commun. 2024 Apr 20;15(1):3375. doi: 10.1038/s41467-024-47840-1.

DOI:10.1038/s41467-024-47840-1
PMID:38643254
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11032393/
Abstract

Cellular and organismal aging have been consistently associated with mitochondrial dysfunction and inflammation. Accumulating evidence indicates that aging-related inflammatory responses are mechanistically linked to compromised mitochondrial integrity coupled with mtDNA-driven CGAS activation, a process that is tonically inhibited by mitophagy.

摘要

细胞和机体衰老一直与线粒体功能障碍和炎症有关。越来越多的证据表明，与衰老相关的炎症反应在机制上与受损的线粒体完整性以及 mtDNA 驱动的 CGAS 激活有关，这一过程受到自噬的紧张抑制。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0540/11032393/e7684be6fd04/41467_2024_47840_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0540/11032393/e7684be6fd04/41467_2024_47840_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0540/11032393/e7684be6fd04/41467_2024_47840_Fig1_HTML.jpg

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