Journal
FRONTIERS IN AGING
Volume 3, Issue -, Pages -Publisher
FRONTIERS MEDIA SA
DOI: 10.3389/fragi.2022.926627
Keywords
RPE; aging; degeneration; mitochondria; senescense; cell death; age-related macula degeneration
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Funding
- YT was supported by American Federation for Aging Research (AFAR) Scholarship. SW was supported by a Startup fund from Tulane University, BrightFocus Foundation Grant in AMD, and NIH Grants EY021862 and EY026069. The fundings are not responsible for the co
- American Federation for Aging Research (AFAR) Scholarship
- Tulane University
- BrightFocus Foundation Grant in AMD [EY021862, EY026069]
- NIH
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This article summarizes the important functions of retinal pigment epithelial (RPE) cells and the role of mitochondria in aging and age-related diseases. The current research efforts to prevent or treat RPE degeneration by restoring mitochondrial function and dynamics are also discussed.
Retinal pigment epithelial (RPE) cells form a monolayer between the neuroretina and choroid. It has multiple important functions, including acting as outer blood-retina barrier, maintaining the function of neuroretina and photoreceptors, participating in the visual cycle and regulating retinal immune response. Due to high oxidative stress environment, RPE cells are vulnerable to dysfunction, cellular senescence, and cell death, which underlies RPE aging and age-related diseases, including age-related macular degeneration (AMD). Mitochondria are the powerhouse of cells and a major source of cellular reactive oxygen species (ROS) that contribute to mitochondrial DNA damage, cell death, senescence, and age-related diseases. Mitochondria also undergo dynamic changes including fission/fusion, biogenesis and mitophagy for quality control in response to stresses. The role of mitochondria, especially mitochondrial dynamics, in RPE aging and age-related diseases, is still unclear. In this review, we summarize the current understanding of mitochondrial function, biogenesis and especially dynamics such as morphological changes and mitophagy in RPE aging and age-related RPE diseases, as well as in the biological processes of RPE cellular senescence and cell death. We also discuss the current preclinical and clinical research efforts to prevent or treat RPE degeneration by restoring mitochondrial function and dynamics.
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