ROS production and mitochondrial dysfunction driven by PU.1-regulated NOX4-p22phox activation in A β -induced retinal pigment epithelial cell injury

Conclusion: 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.
Source: Theranostics - Category: Molecular Biology Authors: Tags: Research Paper Source Type: research