Endoplasmic reticulum stress in the pathogenesis of age-related macular degeneration
10.3980/j.issn.1672-5123.2022.2.14
- VernacularTitle:内质网应激在年龄相关性黄斑变性中的研究进展
- Author:
Xia Liu
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Author Information
1. Department of Ophthalmology, Fourth Affiliated Hospital of Kunming Medical University
2. Department of Ophthalmology, the Second People'
3. s Hospital of Yunnan Province
4. Yunnan Eye Institute
5. The Ocular Disease and Clinical Medicine Research Center of Yunnan Province
6. The Ocular Disease Clinical Medicine Center of Yunnan Province
7. Key Laboratory of Yunnan Province for the Prevention and Treatment of Ophthalmology
8. Expert Workstation of Yao Ke, Kunming 650021, Yunnan Province, China
- Publication Type:Review
- Keywords:
age-related macular degeneration;
endoplasmic reticulum stress;
unfolded protein response;
retinal pigment epithelium cells;
apoptosis
- From:
International Eye Science
2022;22(2):244-248
- CountryChina
- Language:Chinese
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Abstract:
Age-related macular degeneration(ARMD)is a main cause of irreversible visual impairment in the elderly. The major pathological features are drusen formation, macular pigment disorder, geographic atrophy and abnormal neovascularization. Retinal pigment epithelium(RPE)function is impaired in ARMD. Endoplasmic reticulum(ER)is an organelle in eukaryotes responsible for protein synthesis, modification, integration and quality control. ER also participates in the maintenance of calcium homeostasis and lipid biosynthesis. Stimuli from the external and internal environment may trigger ER stress and therefore activate the intracellular signal transduction pathway-the unfolded protein response(UPR), to restore cell homeostasis. However, prolonged ER stress may lead to apoptosis. The pathogenesis of ARMD has not been fully elucidated, nevertheless, compelling evidence demonstrates that ER stress is involved. In this article, we summarize recent advances in UPR pathways, as well as the role of ER stress in the physiological function of RPE and in the pathogenesis of ARMD.
- Full text:202202014.pdf
