Regulation of epithelial-mesenchymal transition in retinal pigment epithelium and its associated cellular signaling cascades: an updated review

Abstract

Abstract Background The epithelial-mesenchymal transition (EMT) affects the retinal pigment epithelium's natural homeostasis. According to observations from around the world, numerous oculopathies, including proliferative vitreoretinopathy (PVR), diabetic retinopathy (DR), and other macular degenerative illnesses such as age-related macular degeneration (AMD), have been linked to the epithelial-mesenchymal transition of retinal pigment epithelium (EMT of RPE). Retinopathy is referred to as an impairment in the retina, where AMD is characterized as an alteration in the macula region, DR as an impairment in the microvascular system, and PVR as an alteration in the subretinal bands, fibrovascular membranes, and fibrotic alteration in the detached retina. To find molecular targets and therapeutic drugs to protect and restore RPE function, a connection between EMT-related signaling pathways and RPE degeneration must be established. Main body of abstract Studies conducted in vivo and in vitro indicate that several signaling pathways, including the Rho pathway, the transforming growth factor-β (TGFβ) pathway, the Jagged/Notch pathway, mitogen-activated protein kinase (MAPK)-dependent pathway, and Wnt/β-catenin pathway, are activated in RPE cells during PVR and AMD. In order to discover the most suitable candidate for retinopathy therapies, it is necessary to determine the relationship between the regulators of the EMT and the degeneration of the RPE. To treat retinopathies, particularly those that are brought on by the EMT of retinal pigment epithelial cells, it is necessary to investigate prospective pharmaceutical candidates. Conclusion TGFβ's intracellular cascade, which comprises both canonical (SMAD-associated) and non-canonical (SMAD-nonassociated) pathways, is shown to be the most active signaling pathway in the degeneration of the RPE caused by EMT.