Diabetic Retinopathy: New Treatment Approaches Targeting Redox and Immune Mechanisms

Abstract

Diabetic retinopathy (DR) represents a severe complication of diabetes mellitus, characterized by irreversible visual impairment resulting from microvascular abnormalities. Since the global prevalence of diabetes continues to escalate, DR has emerged as a prominent area of research interest. The development and progression of DR encompass a complex interplay of pathological and physiological mechanisms, such as high glucose-induced oxidative stress, immune responses, vascular endothelial dysfunction, as well as damage to retinal neurons. Recent years have unveiled the involvement of genomic and epigenetic factors in the formation of DR mechanisms. At present, extensive research explores the potential of biomarkers such as cytokines, molecular and cell therapies, antioxidant interventions, and gene therapy for DR treatment. Notably, certain drugs, such as anti-VEGF agents, antioxidants, inhibitors of inflammatory responses, and protein kinase C (PKC)-β inhibitors, have demonstrated promising outcomes in clinical trials. Within this context, this review article aims to introduce the recent molecular research on DR and highlight the current progress in the field, with a particular focus on the emerging and experimental treatment strategies targeting the immune and redox signaling pathways.

Cancer to Cataracts: The Mechanistic Impact of Aldo-Keto Reductases in Chronic Diseases

“…Vascular Endothelial Growth Factor (VEGF) promotes retinal blood vessel growth, a key DR development factor. Animal studies show that AKR1B1 null mutation reduces VEGF elevation in the diabetic retina, preventing blood-retinal barrier (BRB) breakdown and retinal apoptosis [ 71 ]. This deletion also protects mice from streptozotocin-induced DR by inhibiting retinal capillary degeneration and superoxide generation.…”