BMPR1A promotes ID2–ZEB1 interaction to suppress excessive endothelial to mesenchymal transition
Name
cvac159.pdf
Description
Published version
Size
16.4 MB
Format
Adobe PDF
Checksum (MD5)
47abab153aedd4e768bb7ca1cdef2558
Author(s)
Lee, Heon-Woo
Adachi, Takaomi
Pak, Boryeong
Park, Saejeong
Hu, Xiaoyue
Choi, Woosoung
Kowalski, Piotr S
Chang, C Hong
Clapham, Katharine R
Lee, Aram
Date Issued
May 2, 2023
Journal
Cardiovascular Research
Publisher
Oxford University Press
Citation
Heon-Woo Lee, Takaomi Adachi, Boryeong Pak, Saejeong Park, Xiaoyue Hu, Woosoung Choi, Piotr S Kowalski, C Hong Chang, Katharine R Clapham, Aram Lee, Irinna Papangeli, Jongmin Kim, Orjin Han, Jihwan Park, Daniel G Anderson, Michael Simons, Suk-Won Jin, Hyung J Chun, BMPR1A promotes ID2–ZEB1 interaction to suppress excessive endothelial to mesenchymal transition, Cardiovascular Research, Volume 119, Issue 3, March 2023, Pages 813–825.
Version
Final published version
Abstract
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.
MIT Department
Koch Institute for Integrative Cancer Research at MIT
Terms of Use
Article is made available in accordance with the publisher's policy and may be subject to US copyright law. Please refer to the publisher's site for terms of use.
Persistent DSpace Link
DOI of Published Version
https://doi.org/10.1093/cvr/cvac159
