Int J Biol Sci 2021; 17(14):3923-3935. doi:10.7150/ijbs.64953 This issue

Review

Role of mismatch repair in aging

Jie Wen1,2,3,4, Yangyang Wang1,2, Minghao Yuan1,2, Zhenting Huang1,2, Qian Zou1,2, Yinshuang Pu1,2, Bin Zhao3,4✉, Zhiyou Cai1,2✉

1. Chongqing Key Laboratory of Neurodegenerative Diseases, Chongqing, 400013, China.
2. Department of Neurology, Chongqing General Hospital, University of Chinese Academy of Sciences, Chongqing, 400013, China.
3. Department and Institute of Neurology, Guangdong Medical University, Guangdong, 524001, China.
4. Guangdong Key Laboratory of aging related cardio cerebral diseases, Guangdong, 524001, China.

This is an open access article distributed under the terms of the Creative Commons Attribution License (https://creativecommons.org/licenses/by/4.0/). See http://ivyspring.com/terms for full terms and conditions.
Citation:
Wen J, Wang Y, Yuan M, Huang Z, Zou Q, Pu Y, Zhao B, Cai Z. Role of mismatch repair in aging. Int J Biol Sci 2021; 17(14):3923-3935. doi:10.7150/ijbs.64953. Available from https://www.ijbs.com/v17p3923.htm

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Abstract

Graphic abstract

A common feature of aging is the accumulation of genetic damage throughout life. DNA damage can lead to genomic instability. Many diseases associated with premature aging are a result of increased accumulation of DNA damage. In order to minimize these damages, organisms have evolved a complex network of DNA repair mechanisms, including mismatch repair (MMR). In this review, we detail the effects of MMR on genomic instability and its role in aging emphasizing on the association between MMR and the other hallmarks of aging, serving to drive or amplify these mechanisms. These hallmarks include telomere attrition, epigenetic alterations, mitochondrial dysfunction, altered nutrient sensing and cell senescence. The close relationship between MMR and these markers may provide prevention and treatment strategies, to reduce the incidence of age-related diseases and promote the healthy aging of human beings.

Keywords: aging, mismatch repair, genomic instability, telomere attrition, epigenetic alterations, mitochondrial dysfunction