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Schematic illustration of the potential mechanisms underlying EMT in RPE cells. (A) Loss of ZO-1 and E-cadherin lead to a release of ZONAB and β-catenin. (B) Accumulation of misfolded proteins activate NK/p38-MAPK pathway that crosstalks with TGF-β-induced non-Smad pathways in an IRE-dependent manner. (C) Increased production of TGF-β is associated with inflammation and injury in RPE cells. (D) Above signals promote EMT by upregulating EMT drivers including Snail, Zeb and bHLH family.
