Mitochondria as a sensor, a central hub and a biological clock in psychological stress-accelerated aging.

Xuyun Liu, Xing Zhang, Lin Zhao, Jiangang Long, Zhihui Feng, Jiacan Su, Feng Gao, Jiankang Liu

Journal: Ageing research reviews 2024;93():102145

PMID: 38030089

Full Text on Elsevier Science View on PubMed

Abstract

The theory that oxidative damage caused by mitochondrial free radicals leads to aging has brought mitochondria into the forefront of aging research. Psychological stress that encompasses many different experiences and exposures across the lifespan has been identified as a catalyst for accelerated aging. Mitochondria, known for their dynamic nature and adaptability, function as a highly sensitive stress sensor and central hub in the process of accelerated aging. In this review, we explore how mitochondria as sensors respond to psychological stress and contribute to the molecular processes in accelerated aging by viewing mitochondria as hormonal, mechanosensitive and immune suborganelles. This understanding of the key role played by mitochondria and their close association with accelerated aging helps us to distinguish normal aging from accelerated aging, correct misconceptions in aging studies, and develop strategies such as exercise and mitochondria-targeted nutrients and drugs for slowing down accelerated aging, and also hold promise for prevention and treatment of age-related diseases.

Address: Center for Mitochondrial Biology and Medicine, The Key Laboratory of Biomedical Information Engineering of Ministry of Education, School of Life Science and Technology, Xi'an Jiaotong University, Xi'an 710049, China. Electronic address: [email protected].; Key Laboratory of Ministry of Education, School of Aerospace Medicine, Fourth Military Medical University, Xi'an 710032, China. Electronic address: [email protected].; Cardiometabolic Innovation Center, Ministry of Education, Department of Cardiology, First Affiliated Hospital of Xi'an Jiaotong University, Xi'an 710061, China. Electronic address: [email protected].; Center for Mitochondrial Biology and Medicine, The Key Laboratory of Biomedical Information Engineering of Ministry of Education, School of Life Science and Technology, Xi'an Jiaotong University, Xi'an 710049, China. Electronic address: [email protected].; Center for Mitochondrial Biology and Medicine, The Key Laboratory of Biomedical Information Engineering of Ministry of Education, School of Life Science and Technology, Xi'an Jiaotong University, Xi'an 710049, China. Electronic address: [email protected].; Department of Orthopedics, Xinhua Hospital Affiliated to Shanghai JiaoTong University School of Medicine, Shanghai 200092, China; National Center for Translational Medicine (Shanghai) SHU Branch, Shanghai University, Shanghai 200444, China. Electronic address: [email protected].; Key Laboratory of Ministry of Education, School of Aerospace Medicine, Fourth Military Medical University, Xi'an 710032, China. Electronic address: [email protected].; Center for Mitochondrial Biology and Medicine, The Key Laboratory of Biomedical Information Engineering of Ministry of Education, School of Life Science and Technology, Xi'an Jiaotong University, Xi'an 710049, China; School of Health and Life Sciences, University of Health and Rehabilitation Sciences, Qingdao 266071, China. Electronic address: [email protected].

DOI: 10.1016/j.arr.2023.102145

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MeSH Terms: Humans, Aging, Oxidative Stress, Mitochondria, Free Radicals, Biological Clocks