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. 2022 Sep 21;16:968369. doi: 10.3389/fnhum.2022.968369

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Copyright © 2022 Shabani, Schuerger and Su.

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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Schematic representation of the effects ECs and vSMCs on bAVM development. ENG and ALK1 are receptors of BMPs. TGF-β interacts with ALK5 and TGF-βR that are predominantly expressed in ECs. BMP9/10-ENG-ALK1 by triggering SMAD1,5,8, and 4 regulate angiogenesis and vascular maturation. Disruption of this pathway can cause the development of bAVMs. ANGPT/Tie2 are linked to TGF-β activation and binding to TGF-βR, which through SMAD2,3, and 4 induces angiogenesis. EphrinB2/EphrinB4 are differentially expressed in arterial and venous ECs. PDGFB and PDGFR-β both have an essential role in pericyte recruitment during angiogenesis. In the vSMCs, PDGFB upregulates ANGPT-1 through PI3K and PKC pathway and upregulates TGF-β1 expression through the MAPK pathway. ANGPT-1: angiopoietin 1, PDGFB: platelet derived growth factor B, PDGFR-β: PDGF receptor β, ECs: endothelial cells, SMCs: smooth muscle cells.