PRDX2 and Müller cells in diabetic retinopathy

Figure 1 Proposed model of peroxiredoxin-2-induced Müller cell impairment in diabetic retinopathy. Chronic hyperglycemia enhances oxidative stress and stimulates the upregulation of peroxiredoxin-2 (PRDX2) in Müller glial cells. In pathological conditions, PRDX2 appears to relieve RhoGDI1-mediated inhibition of RhoA, thereby activating the RhoA/ROCK pathway. This axis promotes cytoskeletal reshaping, Müller cell reactive gliosis, inflammatory signaling, and disruption of neurovascular equilibrium. Together, these processes lead to the breakdown of the blood-retinal barrier, vascular leakage, retinal neurodegeneration, and progression of diabetic retinopathy. PRDX2: Peroxiredoxin-2.