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视网膜代谢重编程在视网膜退行性疾病中的机制研究进展

陈中昱 刘瑞宝 黄琴 霍勤

眼科新进展2026,Vol.46Issue(9):746-751,6.
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眼科新进展2026,Vol.46Issue(9):746-751,6.DOI:10.13389/j.cnki.rao.2026.0129

视网膜代谢重编程在视网膜退行性疾病中的机制研究进展

Research progress on the mechanisms of retinal metabolic reprogramming in retinal degenerative diseases

陈中昱 1刘瑞宝 2黄琴 3霍勤2

作者信息

  • 1. 450000 河南省郑州市,河南中医药大学第一临床医学院||450000 河南省郑州市,河南中医药大学第一附属医院
  • 2. 450000 河南省郑州市,河南中医药大学第一附属医院
  • 3. 450000 河南省郑州市,河南中医药大学第一临床医学院
  • 折叠

摘要

Abstract

Retinal degenerative diseases are a leading cause of irreversible vision loss,and their pathological processes are closely associated with metabolic homeostasis imbalances in retinal cells.Retinal metabolic reprogramming,as a core mechanism by which cells adapt to stress and maintain function and survival,has become a key entry point for understand-ing disease pathogenesis and exploring therapeutic strategies.This review summarizes the latest advances in this field,with a focus on the metabolic reprogramming of Müller cells and its epigenetic regulatory mechanisms,the association between mi-tochondrial autophagy and metabolic remodeling in retinal pigment epithelial cells,exosome-mediated intercellular metabolic signaling in hypoxic microenvironments,and Müller cell reprogramming based on non-human primate models.By systemati-cally elucidating these molecular and cellular mechanisms,this review highlights the critical role of metabolic reprogram-ming in the progression of retinal degenerative diseases,providing a theoretical foundation and new perspectives for the de-velopment of innovative therapeutic strategies targeting metabolic pathways.

关键词

视网膜代谢重编程/视网膜退行性疾病/Müller胶质细胞/外泌体/表观遗传调控

Key words

retinal metabolic reprogramming/retinal degenerative diseases/Müller glial cells/exosomes/epigenetic regulation

分类

医药卫生

引用本文复制引用

陈中昱,刘瑞宝,黄琴,霍勤..视网膜代谢重编程在视网膜退行性疾病中的机制研究进展[J].眼科新进展,2026,46(9):746-751,6.

基金项目

河南省自然科学基金项目(编号:252300421629) (编号:252300421629)

河南省中医药科学研究专项课题(编号:2024ZY2043,2022ZY1010,2022JDZX023) (编号:2024ZY2043,2022ZY1010,2022JDZX023)

眼科新进展

1003-5141

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