BMPR1A promotes ID2–ZEB1 interaction to suppress excessive endothelial to mesenchymal transition

BMPR1A promotes ID2–ZEB1 interaction to suppress excessive endothelial to mesenchymal transition

Components of bone morphogenetic protein (BMP) signalling have been implicated in both pathogenesis of pulmonary arterial hypertension (PAH) and endothelial-mesenchymal transition (EndoMT). In particular, the importance of BMP type 2 receptor in these processes has been extensively analysed. However...

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Bibliographic Details
Main Authors: Lee, Heon-Woo, Adachi, Takaomi, Pak, Boryeong, Park, Saejeong, Hu, Xiaoyue, Choi, Woosoung, Kowalski, Piotr S, Chang, C Hong, Clapham, Katharine R, Lee, Aram, Papangeli, Irinna, Kim, Jongmin, Han, Orjin, Park, Jihwan, Anderson, Daniel G, Simons, Michael, Jin, Suk-Won, Chun, Hyung J
Other Authors: Koch Institute for Integrative Cancer Research at MIT
Format: Article
Language:English
Published: Oxford University Press 2024
Online Access:https://hdl.handle.net/1721.1/156912
Description
Summary:Components of bone morphogenetic protein (BMP) signalling have been implicated in both pathogenesis of pulmonary arterial hypertension (PAH) and endothelial-mesenchymal transition (EndoMT). In particular, the importance of BMP type 2 receptor in these processes has been extensively analysed. However, the contribution of BMP type 1 receptors (BMPR1s) to the onset of PAH and EndoMT remains poorly understood. BMPR1A, one of BMPR1s, was recently implicated in the pathogenesis of PAH, and was found to be down-regulated in the lungs of PAH patients, neither the downstream mechanism nor its contribution to EndoMT has been described. Therefore, we aim to delineate the role of endothelial BMPR1A in modulating EndoMT and pathogenesis of PAH.

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