期刊
AGING AND DISEASE
卷 -, 期 -, 页码 -出版社
INT SOC AGING & DISEASE
DOI: 10.14336/AD.2022.1217
关键词
ATF7; cellular senescence; H3K9me2; longevity; NF-kappa B
资金
- National Key R&D Program of China [2018YFC2000400, 2018YFE0203700, 2021YFF1201200]
- CAS Project for Young Scientists in Basic Research [YSBR-076]
- Key Research Program [KFZD-SW-221]
- West Light Foundation
- Pioneer Hundred Talents Program of the Chinese Academy of Sciences
- National Natural Science Foundation of China [82071595, 82171558]
- Basic Research Projects of Yunnan Province [202101AT070299, 202101AS070058, 202201AS070080, 202101AS070137]
- High-level Talent Promotion and Training Project of Kunming (Spring City Plan) [2020SCP001]
- Project Program of National Clinical Research Center for Geriatric Disorders (Xiangya Hospital) [2021LNJJ03]
- Yunling Scholar of Yunnan Province
This study found that long-lived individuals have lower inflammation levels and up-regulation of ATF7. Overexpression of ATF7 can delay cellular senescence and inhibit inflammation, thus promoting longevity.
Aging is characterized by persistent low-grade systematic inflammation, which is largely responsible for the occurrence of various age-associated diseases. We and others have previously reported that long-lived people (such as centenarians) can delay the onset of or even escape certain major age-related diseases. Here, by screening blood transcriptome and inflammatory profiles, we found that long-lived individuals had a relatively lower inflammation level (IL6, TNFa), accompanied by up-regulation of activating transcription factor 7 (ATF7). Interestingly, ATF7 expression was gradually reduced during cellular senescence. Loss of ATF7 induced cellular senescence, while overexpression delayed senescence progress and senescence-associated secretory phenotype (SASP) secretion. We showed that the anti-senescence effects of ATF7 were achieved by inhibiting nuclear factor kappa B (NF-.B) signaling and increasing histone H3K9 dimethylation (H3K9me2). In Caenorhabditis elegans, ATF7 overexpression significantly suppressed aging biomarkers and extended lifespan. Our findings suggest that ATF7 is a longevity-promoting factor that lowers cellular senescence and inflammation in long-lived individuals.
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