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. 2018 Sep 24;1:149. doi: 10.1038/s42003-018-0152-1

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© The Author(s) 2018

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.

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Fig. 7 — Schematic diagram of the maintenance of RAD51 by the BMP9–ALK-1/BMPR2 signaling axis. In healthy individuals, RAD51 is maintained in the pulmonary endothelium as the BMP9–ALK-1/BMPR2 signaling axis downregulates miR-96 expression and prevents the destabilization of RAD51 mRNA. When the BMP9–ALK-1/BMPR2 signaling axis is deregulated, elevation of miR-96 leads to attenuation of RAD51. As a result, DNA damage accumulates in the pulmonary endothelium over several decades causing endothelial injury and dysfunction, and eventually triggers pulmonary vascular remodeling