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Bone morphogenetic protein-9 controls pulmonary vascular growth and remodeling

Pulmonary arterial hypertension (PAH) and hereditary hemorrhagic telangiectasia (HHT) are two distinct vascular diseases linked to impaired signaling through bone morphogenetic protein (BMP) receptor complexes in endothelial cells. Although BMP-9 plays a central role in activating this pathway by binding to ALK1 and BMPR-­II, its precise function in the pulmonary microvasculature has remained unclear. In this study, we uncover a previously unrecognized role for BMP-9 in regulating pulmonary vascular architecture and homeostasis. Our findings demonstrate that BMP-9 signaling intersects with VEGF pathways and contributes to the delicate balance between vascular growth and remodeling in the lungs. We also show that disruption of this pathway can shift vascular responses toward an HHT-­like state, potentially altering disease susceptibility. These insights offer a unique perspective on how BMP-9 and ALK1 shape pulmonary vascular biology and suggest that targeting this axis could inform future strategies for treating complex vascular diseases such as PAH.

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Studies are experimental investigations of a particular phenomenon, e.g., case-control studies on a particular trait or cancer research projects reporting matching cancer normal genomes from patients.

Study ID Study Title Study Type
EGAS50000001026 Transcriptome Analysis

This table displays only public information pertaining to the files in the dataset. If you wish to access this dataset, please submit a request. If you already have access to these data files, please consult the download documentation.

ID File Type Size Quality Report
Located in
EGAF00008740614 bam 32.7 GB
EGAF00008740615 bam 34.4 GB
EGAF00008740616 bam 35.7 GB
EGAF00008740617 bam 34.5 GB
EGAF00008740618 bam 35.5 GB
5 Files (172.7 GB)