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. 2020 Mar 11;11(3):516–526. doi: 10.1111/jdi.13219

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© 2020 The Authors. Journal of Diabetes Investigation published by Asian Association for the Study of Diabetes (AASD) and John Wiley & Sons Australia, Ltd

This is an open access article under the terms of the http://creativecommons.org/licenses/by-nc/4.0/ License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited and is not used for commercial purposes.

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N‐acetyl‐seryl‐aspartyl‐lysyl‐proline (AcSDKP)–fibroblast growth factor receptor 1 (FGFR1)–mitogen‐activated protein kinase kinase kinase kinase 4 (MAP4K4) axis‐induced suppression of integrin–transforming growth factor‐β receptors (TGFβRs) interaction and endothelial mesenchymal transition (EndMT). AcSDKP shows close proximity and would stabilize FGFR1. Alternatively, AcSDKP suppresses interferon‐γ (IFN‐γ), which inhibits FGFR1 levels in endothelial cells. FGFR1 physically interacts with MAP4K4 by which integrin β1 signaling is suppressed. Integrin β1 is essential for the heterodimer formations of TGFβRs; integrin β1 suppression directly results in the suppression of TGF‐β1‐smad signaling and EndMT.