Targeting Genome Stability to Mitigate Human Aging and Disease.
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The maintenance of a stable genome requires constant repair.
APA
Toiber D, Schumacher B (2026). Targeting Genome Stability to Mitigate Human Aging and Disease.. Annual review of pathology, 21(1), 213-238. https://doi.org/10.1146/annurev-pathmechdis-042624-105942
MLA
Toiber D, et al.. "Targeting Genome Stability to Mitigate Human Aging and Disease.." Annual review of pathology, vol. 21, no. 1, 2026, pp. 213-238.
PMID
41086257 ↗
Abstract 한글 요약
The maintenance of a stable genome requires constant repair. Congenital DNA repair defects lead to cancer susceptibility and progeroid (premature aging-like) syndromes. Even with intact repair, DNA lesions accumulate in aging organisms, leading to replication and transcription stress and age-dependent somatic mutations. These, in turn, can compromise cellular function and elevate cancer risk. DNA damage response (DDR) mechanisms can lead to cellular death and senescence, and targeting the DDR has emerged as therapeutic strategy not only in cancer but also to protect from age-associated phenotypes. Inhibiting DNA repair can promote cancer cell death. Eliminating senescent cells may alleviate proinflammatory consequences on their tissue environment. Moreover, strategies to limit DNA damage and augment repair in normal cells are in active development. Here, we review emerging concepts for targeting genome maintenance mechanisms to lower cancer risk and lengthen healthy lifespan by extending the integrity and functionality of somatic genomes.
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