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The ticking of aging clocks
1Peking-Tsinghua Center for Life Sciences, Academy for Advanced Interdisciplinary Studies, Center for Quantitative Biology (CQB), Peking University, Beijing, China; Peking University Chengdu Academy for Advanced Interdisciplinary Biotechnologies, Chengdu, China; International Center for Aging and Cancer (ICAC), The First Affiliated Hospital, Hainan Medical University, Haikou, China.
Trends in Endocrinology and Metabolism: TEM
|October 25, 2023
Summary
Aging clocks measure biological age, but their timers are unclear. This research proposes DNA damage as a fundamental counting unit for aging, impacting cellular senescence and tissue decline.
Area of Science:
- Gerontology
- Molecular Biology
- Cellular Biology
Background:
- Aging clocks estimate biological age independently of chronological age.
- The precise mechanisms underlying aging clocks remain largely unknown.
- Key aging factors include DNA damage, epigenetic alterations, and inflammation.
Purpose of the Study:
- To explore the fundamental counting mechanisms of aging clocks.
- To investigate the role of DNA damage as a potential aging timer.
- To identify key intervention points for aging processes.
Main Methods:
- Review of molecular mediators of aging.
- Analysis of the relationship between DNA damage, cellular senescence, and inflammation.
- Discussion of DNA damage response pathways.
Main Results:
- Persistent DNA damage triggers cellular senescence and the senescence-associated secretory phenotype (SASP).
- SASP promotes immune cell infiltration, which can exacerbate DNA damage via reactive oxygen and nitrogen species (RONS).
- DNA damage and its response may serve as the fundamental counting unit for cellular aging.
Conclusions:
- DNA damage is a strong candidate for the fundamental counting unit in cellular aging and senescence.
- Understanding this mechanism could reveal critical intervention points for age-related decline.
- This perspective integrates DNA damage, epigenetics, and inflammation in aging processes.
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