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Updated: Feb 10, 2026

Author Spotlight: Exploring the Impact of Trauma on Cellular Aging
Published on: March 22, 2024
[ATM and telomere instability]
Hong-Mei Wang1, Yun-Fei Xia, Xin-Yao Wu
1Department of Forensic Medicine, Sun Yat-Sen University, Guangzhou 510080, China.
Abstract:
Accumulation of DNA damage has been associated with the onset of senescence and the predisposition to cancer. The gene responsible for ataxia telangiectasia (A-T) is ATM (Ataxia-telangiectasia mutant), a master controller of cellular pathways and networks, orchestrating the response to a specific type of DNA damage, i.e., the double strand break. It has now been demonstrated that mutations in ATM lead to defective telomere maintenance in mammalian cells. This review will focus on its roles in telomere metabolism and how ATM and telomeres serve as controllers of cellular responses to DNA damage.
Insights
DNA damage accumulation links to aging and cancer. Mutations in the Ataxia-telangiectasia mutated (ATM) gene impair telomere maintenance, impacting cellular responses to DNA damage.
Area of Science:
- Genetics
- Cell Biology
- Molecular Biology
Background:
- DNA damage accumulation is linked to cellular senescence and cancer.
- The Ataxia-telangiectasia mutated (ATM) gene is crucial for responding to DNA double-strand breaks.
- ATM acts as a central regulator of cellular pathways.
Purpose of the Study:
- To review the role of ATM in telomere metabolism.
- To explore how ATM and telomeres control cellular responses to DNA damage.
Main Methods:
- Literature review focusing on ATM gene function.
- Analysis of studies on telomere maintenance and DNA damage response pathways.
Main Results:
- Mutations in ATM disrupt normal telomere maintenance in mammalian cells.
- ATM plays a significant role in regulating telomere stability.
Conclusions:
- ATM is a key controller of cellular responses to DNA damage, including its impact on telomere metabolism.
- Understanding ATM and telomere interactions is vital for addressing age-related diseases and cancer.
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