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. 2021 Feb 8;22(4):1684. doi: 10.3390/ijms22041684

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© 2021 by the authors.

Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (http://creativecommons.org/licenses/by/4.0/).

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ROS-induced EMT-triggered signal propagation and transduction: an intricate interplay in the RPE of NFE2L2/PGC-1α double knockout model enhances epithelial-mesenchymal transition (EMT). Simplified representation of the oxidative stress (OS)-dependent major molecular mechanisms of EMT. Reprogramming of gene expression during EMT, and non-transcriptional changes, are initiated and controlled by signaling pathways that respond to extracellular cues. Here, the arrows pointing from the signaling routes to the EMT transcription factors in the nucleus are grouped. EMT involves a functional transition of highly polarized retinal epithelial cells into ECM component-secreting mesenchymal-type flattened cells. Identification of all mesenchymal cells originating from the RPE via EMT is hardly possible as many mesenchymal cells display some epithelial markers while a transition is not fully completed.