The intervention of epithelial-mesenchymal transition in homeostasis of human retinal pigment epithelial cells: a review

The health and activity of photoreceptors and Bruch's membrane are promoted by the retinal pigment epithelium (RPE), which is essential for normal vision. Age-related macular degeneration (AMD), diabetic retinopathy (DR), and proliferative vitreoretinopathy (PVR) are examples of retinopathies that result in vision loss. Epithelial-mesenchymal transition (EMT) is a process in which epithelial cells transform into mesenchymal cells as a result of a faulty microenvironment, and it is associated with the oculopathies stated above. Cell differentiation, autophagy, growth factors (GFs), the blood-retinal barrier (BRB), and other complicated signaling pathways all contribute to proper morphology, and their disruption by harmful compounds has an impact on RPE function. The inducer and suppressor of EMT in RPE, on the other hand, are unknown. The current article reviews the experimental research investigations, suggested that certain modulators like glucosamine (Glc-N) and bradykinin (BK) suppress the TGFβ signaling pathway and that other variables like oxidative stress triggered EMT, which is not found in normal RPE homeostasis. Finding molecular targets and treatments to prevent and restore RPE function, as well as understanding how EMT regulators affect RPE degeneration, are therefore crucial.