Author: Lanlan Zhang1, Jianlong Wu1, Ziguan Zhu1, Yuchen He2, Renpeng Fang3
1 Center for Plastic & Reconstructive Surgery, Department of Hand & Reconstructive Surgery, Zhejiang Provincial People's Hospital, Affiliated People's Hospital, Hangzhou Medical College, Hangzhou, Zhejiang, China.
2 Department of Orthopaedic Surgery, University of Pittsburgh School of Medicine, Pittsburgh, PA 15219, USA; Department of Orthopaedics, the Second Xiangya Hospital, Central South University, Changsha, Hunan, China.
3 Center for Plastic & Reconstructive Surgery, Department of Hand & Reconstructive Surgery, Zhejiang Provincial People's Hospital, Affiliated People's Hospital, Hangzhou Medical College, Hangzhou, Zhejiang, China. Electronic address: firstname.lastname@example.org.
Conference/Journal: Life Sci
Date published: 2023 Apr 6
Other: Special Notes: doi: 10.1016/j.lfs.2023.121666. , Word Count: 155
Aging is a natural process, characterized by progressive loss of physiological integrity, impaired function, and increased vulnerability to death. For centuries, people have been trying hard to understand the process of aging and find effective ways to delay it. However, limited breakthroughs have been made in anti-aging area. Since the hallmarks of aging were summarized in 2013, increasing studies focus on the role of mitochondrial dysfunction in aging and aging-related degenerative diseases, such as neurodegenerative diseases, osteoarthritis, metabolic diseases, and cardiovascular diseases. Accumulating evidence indicates that restoring mitochondrial function and biogenesis exerts beneficial effects in extending lifespan and promoting healthy aging. In this paper, we provide an overview of mitochondrial changes during aging and summarize the advanced studies in mitochondrial therapies for the treatment of degenerative diseases. Current challenges and future perspectives are proposed to provide novel and promising directions for future research.
Keywords: Aging; Degenerative diseases; Longevity; Mitochondrion; Mitochondrion-nuclear communication; Mitophagy.
PMID: 37030614 DOI: 10.1016/j.lfs.2023.121666