PRDX4 mitigates diabetic retinopathy by inhibiting reactive gliosis, apoptosis, ER stress, oxidative stress, and mitochondrial dysfunction in Muller cells.

ABSTRACT: Diabetic retinopathy (DR) is a neurovascular complication of diabetes. As a crucial player in the retinal physiology, Müller cells are affected in DR, impairments of Müller cell function lead to retinal malfunctions. Therefore, searching for approaches to mitigate diabetes-induced injury in Müller cells is imperative for delaying DR. Peroxiredoxin 4 (PRDX4), an important endoplasmic reticulum (ER)-resident antioxidant, was explored in this study for its potential protective role against DR. Streptozotocin-induced mouse model of diabetes and high glucose (HG)-induced Müller cells were utilized to assess the impact of PRDX4. Compared with WT mice, PRDX4 knockout exacerbated retinal neurodegeneration, reactive gliosis, cell apoptosis, ER stress, oxidative stress, and mitochondrial dysfunction

SUBMITTER: Huang Y 

PROVIDER: S-EPMC11760821 | biostudies-literature | 2025 Jan

REPOSITORIES: biostudies-literature