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. 2020 May 5;7:53. doi: 10.3389/fcvm.2020.00053

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Copyright © 2020 Chen, Schwartz and Simons.

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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Inflammation and endothelial-to-mesenchymal transition (EndMT). Inflammatory mediators including interferon γ (IFN-γ), tumor necrosis factor α (TNF-α), and interleukin 1β (IL-1β) induce downregulation of endothelial fibroblast growth factor (FGF) receptors, reducing FGF signaling input. This leads to a large fall in let-7 miRNA levels and activation of transforming growth factor receptor β (TGFβ) signaling, initiating EndMT. Restoration of FGF signaling, endothelial let-7 miRNA levels, or suppression of endothelial TGFβ receptor expression arrest EndMT development.