Research progress of mitochondrial genetics in age-related macular degeneration
10.3760/cma.j.cn115989-20200511-00331
- VernacularTitle:线粒体遗传学机制在年龄相关性黄斑变性中的研究进展
- Author:
Yusong WANG
1
;
Xiaodong SUN
Author Information
1. 上海交通大学附属第一人民医院眼科 上海市眼底病重点实验室，上海 200080
- Keywords:
Mitochondria;
Age-related macular degeneration;
Mitochondrial DNA;
Mitochondrial dysfunction
- From:
Chinese Journal of Experimental Ophthalmology
2023;41(9):949-952
- CountryChina
- Language:Chinese
-
Abstract:
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.
