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Review
. 2025 Aug 1;39(15-16):923-925.
doi: 10.1101/gad.353125.125.

The interplay between senescence, inflammation, and the immune system

Jesús Gil  1
Affiliations
Review

The interplay between senescence, inflammation, and the immune system

Jesús Gil. Genes Dev. .

Abstract

The past 40 years have witnessed significant progress in aging research. Although aging was once considered a stochastic process, it is now understood to be regulated by pathways and processes that can be dissected with modern cellular and molecular biology approaches. The aberrant accumulation of cells undergoing cellular senescence and an increase in chronic, sterile inflammation are two of those aging hallmarks. Here we discuss how these processes are connected and how the relationship between senescent cells and the immune system dictates the extent of inflammatory processes contributing to age-related dysfunction and disease.

Keywords: aging; inflammation; senescence.

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References

    1. Amor C, Feucht J, Leibold J, Ho YJ, Zhu C, Alonso-Curbelo D, Mansilla-Soto J, Boyer JA, Li X, Giavridis T, et al. 2020. Senolytic CAR T cells reverse senescence-associated pathologies. Nature 583: 127–132. 10.1038/s41586-020-2403-9 - DOI - PMC - PubMed
    1. Amor C, Fernández-Maestre I, Chowdhury S, Ho YJ, Nadella S, Graham C, Carrasco SE, Nnuji-John E, Feucht J, Hinterleitner C, et al. 2024. Prophylactic and long-lasting efficacy of senolytic CAR T cells against age-related metabolic dysfunction. Nat Aging 4: 336–349. 10.1038/s43587-023-00560-5 - DOI - PMC - PubMed
    1. Herdy JR, Traxler L, Agarwal RK, Karbacher L, Schlachetzki JCM, Boehnke L, Zangwill D, Galasko D, Glass CK, Mertens J, et al. 2022. Increased post-mitotic senescence in aged human neurons is a pathological feature of Alzheimer's disease. Cell Stem Cell 29: 1637–1652.e6. 10.1016/j.stem.2022.11.010 - DOI - PMC - PubMed
    1. López-Polo V, Maus M, Zacharioudakis E, Lafarga M, Attolini CS, Marques FDM, Kovatcheva M, Gavathiotis E, Serrano M. 2024. Release of mitochondrial dsRNA into the cytosol is a key driver of the inflammatory phenotype of senescent cells. Nat Commun 15: 7378. 10.1038/s41467-024-51363-0 - DOI - PMC - PubMed
    1. Martinez JC, Morandini F, Fitzgibbons L, Sieczkiewicz N, Bae SJ, Meadow ME, Hillpot E, Cutting J, Paige V, Biashad SA, et al. 2024. cGAS deficient mice display premature aging associated with de-repression of LINE1 elements and inflammation. bioRxiv 10.1101/2024.10.10.617645 - DOI

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