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Mitigating age-related somatic mutation burden.

Author information

Affiliations

  • 1. Department of Genetics, Albert Einstein College of Medicine, Bronx, NY 10461, USA; Center for Single-Cell Omics, Shanghai Jiao Tong University School of Medicine, Shanghai 200025, China.
      Authors
    • Vijg J 1
    (1 author)
  • 2. Institute for Genome Stability in Aging and Disease, University and University Hospital of Cologne, Cologne, Germany; Cologne Excellence Cluster for Cellular Stress Responses in Aging-Associated Diseases (CECAD), Center for Molecular Medicine Cologne (CMMC), University of Cologne, Cologne, Germany.
      Authors
    • Schumacher B 2
    (1 author)
  • 3. Altos Labs Cambridge Institute of Science, Granta Park, Cambridge, UK.
      Authors
    • Abakir A 3
    (1 author)
  • 4. Formic Ventures, San Francisco, CA 94107, USA.
      Authors
    • Antonov M 4
    (1 author)
  • 5. Matter Bioworks, Brooklyn, NY 11237, USA.
      Authors
    • Bradley C 5
    • Sharifi S 5
    (2 authors)
    • Show all (13)

ORCIDs linked to this article

Trends in Molecular Medicine, 29 Apr 2023, 29(7):530-540
https://doi.org/10.1016/j.molmed.2023.04.002 PMID: 37121869 

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Abstract 

Genomes are inherently unstable and require constant DNA repair to maintain their genetic information. However, selective pressure has optimized repair mechanisms in somatic cells only to allow transmitting genetic information to the next generation, not to maximize sequence integrity long beyond the reproductive age. Recent studies have confirmed that somatic mutations, due to errors during genome repair and replication, accumulate in tissues and organs of humans and model organisms. Here, we describe recent advances in the quantitative analysis of somatic mutations in vivo. We also review evidence for or against a possible causal role of somatic mutations in aging. Finally, we discuss options to prevent, delay or eliminate de novo, random somatic mutations as a cause of aging.

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Read article at publisher's site: https://doi.org/10.1016/j.molmed.2023.04.002

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Funding 

Funders who supported this work.

Biotechnology and Biological Sciences Research Council (1)

NIA NIH HHS (2)