Research progress of mitochondrial genetics in age-related macular degeneration

Authors: Wang Yusong,  Sun Xiaodong
DOI: 10.3760/cma.j.cn115989-20200511-00331
Published 2023-09-10
Cite as Chin J Exp Ophthalmol, 2023, 41(9): 949-952.

Abstract                              Download PDF】 【Read Full Text

Mitochondria are the center of cellular energy metabolism, and their functions are tightly regulated by the nuclear and mitochondria genomes.Potential mechanisms responsible for age-related mitochondrial dysfunction include the accumulation of mitochondrial DNA (mtDNA) damage caused by replication errors or oxidative damage, and the epigenetic changes in mtDNA (mitoepigenetics). These mechanisms are essential for the development and progression of age-related macular degeneration (AMD). Age-related mtDNA damage disrupts energy metabolism and cellular function in the retinal pigment epithelium (RPE) and neuroretinal cells, which further mediates oxidative stress, lysosomal dysfunction and pyroptosis, resulting in RPE degeneration, drusen deposition and retinal inflammation.Mitochondrial genome protection, such as humanin administration, may be a promising preventive or therapeutic target in the early stages of AMD.This review focused on the research progress of the mitochondrial genetic mechanism in AMD pathogenesis and provided new ideas for exploring the prevention and treatment strategies of AMD.

Key words:

Mitochondria; Age-related macular degeneration; Mitochondrial DNA; Mitochondrial dysfunction

Contributor Information

Wang Yusong

Department of Ophthalmology, Shanghai General Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai Key Laboratory of Fundus Disease, Shanghai 200080, China

Sun Xiaodong

Department of Ophthalmology, Shanghai General Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai Key Laboratory of Fundus Disease, Shanghai 200080, China

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