ROS production and mitochondrial dysfunction driven by PU.1-regulated NOX4-p22<sup>phox</sup> activation in Aβ-induced retinal pigment epithelial cell injury
Junran Sun, Jieqiong Chen, Tong Li, Peirong Huang, Jie Li, Mengxi Shen, Min Gao, Yang Sun, Jian Liang, Xiaomeng Li, Yimin Wang, Yushu Xiao, Xiang Shi, Yifan Hu, Jingyang Feng, Huixun Jia, Te Liu, Xiaodong Sun
Abstract
Our study suggests that PU.1 is a novel therapeutic target for AMD, and the regulation of PU.1 expression represents a potentially novel approach against excessive oxidative stress in Aβ-driven RPE injury.
Topics & Concepts
PigmentNOX4RetinalCell biologyRetinal pigment epitheliumMitochondrionChemistryReactive oxygen speciesBiophysicsBiologyBiochemistryNADPH oxidaseOrganic chemistryNeutrophil, Myeloperoxidase and Oxidative MechanismsRetinal Diseases and TreatmentsAdvanced Glycation End Products research