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Cited by 12Genetics, Aging, and Longevity in Model OrganismsTelomeres, Telomerase, and SenescenceSirtuins and Resveratrol in Medicine

Longevity-Associated Transcription Factor ATF7 Promotes Healthspan by Suppressing Cellular Senescence and Systematic Inflammation

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Huang, Yaqun, Ge, Ming-Xia, Li, Yu-Hong, Li, Jing-Lin, Yu, Qin, Xiao, Fu-Hui, Ao, Hong-Shun, Yang, Li-Qin +3 more·2022·Aging and disease
DOI 10.14336/ad.2022.1217PMC PMC10389835
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Abstract

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, TNFα), 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-κB) 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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  • ATF7 has a role in epigenetic repression of inflammatory pathways and inhibition of NF-kB signaling.

    “This Ts21-specific reduction in ATF7 regulon activity is particularly relevant, given the role of ATF7 in epigenetic repression of inflammatory pathways and inhibition of NF-K β signaling (59), aligning with exacerbated inflammatory signaling in Ts21 astrocytes.”

    From Molecular and cellular processes disrupted in the early postnatal Down syndrome prefrontal cortex (2026) · cites this paper as [59]

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Authors
Huang, Y., Ge, M.-X., Li, Y.-H., Li, J.-L., Yu, Q., Xiao, F.-H., Ao, H.-S., Yang, L.-Q., Li, J., He, Y., & Kong, Q.-P.
Affiliations
  • Central South University (CN)
  • Kunming Institute of Zoology (CN)
Corresponding author
  • Li, Ji
  • He, Yonghan
  • Kong, Qing-Peng
ORCID
Venue
Aging and disease
Publisher
Aging and Disease
Published
2022
Volume
14
Issue
4
Pages
0
ISSN
2152-5250 (ISSN-L)
DOI
10.14336/ad.2022.1217
PMC
PMC10389835
OpenAlex
W4360597856
Cited by
12
References
89
Citations by year
2026: 4 · 2025: 2 · 2024: 2 · 2023: 4
FWCI
0.67
Type
journal article
Language
en
Open access
Licence
cc-by
Locations
  • Aging and Disease (publishedVersion, cc-by)
  • PubMed Central (publishedVersion, cc-by)
  • PubMed (publishedVersion)
Funders
  • National Natural Science Foundation of China (8217155 8, 82071595, 2021-01, 2021YFF1201200, 2018YFC2000400)
  • Chinese Academy of Sciences (KFZD-SW-221, YSBR‐076)
  • Xiangya Hospital, Central South University (2021LNJJ03)
Topics
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Aging › Genetics, Aging, and Longevity in Model Organisms
  • Health Sciences › Medicine › Physiology › Telomeres, Telomerase, and Senescence
  • Health Sciences › Medicine › Geriatrics and Gerontology › Sirtuins and Resveratrol in Medicine
Keywords
ATF7, cellular senescence, healthspan, aging, low-grade inflammation, senescence-associated secretory phenotype, NF-κB signaling, H3K9 dimethylation, centenarians, longevity, lifespan extension, Caenorhabditis elegans, age-related diseases

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