Author:
Gelat Brijesh,Trivedi Krupali,Malaviya Pooja,Rathaur Pooja,Patel Binita,Gelat Rahul,Johar Kaid
Abstract
The retinal pigment epithelium (RPE), which is crucial for good vision, supports the health and function of photoreceptors or Bruch’s membrane (BM). The two most prevalent retinal vascular disorders that account for the majority of blindness in people in their working years and older are diabetic macular edema (DME) and neovascular age-related macular degeneration (nAMD). The blood-retinal barrier (BRB), cell differentiation, autophagy, growth factors (GFs), and other complex signaling pathways all play a role in maintaining morphology, and their disruption by harmful substances affects RPE function. It is urgent to gain a better understanding of the molecular mechanisms underlying the pathogenesis of AMD and identify potential targets as leads for creating potent therapies because there are currently no effective treatments for the early-AMD and late-AMD forms of the disease. For this reason, it is vital to identify molecular targets and therapies that can stop RPE deterioration in AMD and restore RPE function. Currently, the first-line treatment for nAMD and DME involves anti-vascular endothelial growth factor (VEGF) medications that inhibit VEGF family ligands, such as ranibizumab, bevacizumab (off-label usage), brolucizumab, and aflibercept. However, because nAMD and DME have complicated pathophysiological backgrounds, further research is still needed to determine the causes of non-response, resistance to anti-VEGF treatment, and disease relapses.