ArticleFrontiers in genetics2014
Emerging roles of BMP9 and BMP10 in hereditary hemorrhagic telangiectasia.
Article in Frontiers in genetics, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 73 papers.
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Who cites it
73 citing papers in PubMed, 125 citations in OpenAlex.
- A microphysiological system HHT-on-a-chip platform recapitulates patient vascular lesions.Nature communications · 2026Article
- Article
- Endovascular Embolization in Neurovascular Disease: Material Science, Multimodal Management, and Future Horizons.Biomedicines · 2026Review
- Activin Signaling Inhibitors in Pulmonary Hypertension: A State-of-the-Art Review.Pulmonary circulation · 2026Review
- Non-invasive characterization of pericyte dysfunction in mouse brain using functional ultrasound localization microscopy.Nature biomedical engineering · 2026Article
- Characterizing the Microenvironment of Cerebral Arteriovenous Malformations to Test Novel Treatment Modalities.Brain sciences · 2025Review
- The Association of Circulating Bone Morphogenetic Protein 9 and Arterial Stiffness in Hypertensive Patients.Journal of clinical hypertension (Greenwich, Conn.) · 2025Article
- Updates on the Pathogenesis and Therapeutic Approaches for Hereditary Hemorrhagic Telangiectasia.Current vascular pharmacology · 2025Review
- Overlap syndrome of hereditary hemorrhagic telangiectasia and juvenile polyposis syndrome: ten years follow-up-case series and review of literature.Familial cancer · 2024Review
- ACVR1/ALK2-p21 signaling axis modulates proliferation of the venous endothelium in the retinal vasculature.Angiogenesis · 2024Article
- Unveiling the Impact of BMP9 in Liver Diseases: Insights into Pathogenesis and Therapeutic Potential.Biomolecules · 2024Review
- Pathophysiology in Brain Arteriovenous Malformations: Focus on Endothelial Dysfunctions and Endothelial-to-Mesenchymal Transition.Biomedicines · 2024Review
- Bone morphogenetic protein 10, a rising star in the field of diabetes and cardiovascular disease.Journal of cellular and molecular medicine · 2024Review
- Endothelial Function in Pulmonary Arterial Hypertension: From Bench to Bedside.Journal of clinical medicine · 2024Review
- Pulmonary hypertension in hereditary hemorrhagic telangiectasia: A clinical review.Pulmonary circulation · 2023Review
- Aflibercept for Gastrointestinal Bleeding in Hereditary Hemorrhagic Telangiectasia: A Case Report.Medicina (Kaunas, Lithuania) · 2023Article
- Endothelial tip/stalk cell selection requires BMP9-induced βMolecular biology of the cell · 2023Article
- GATA6 coordinates cross-talk between BMP10 and oxidative stress axis in pulmonary arterial hypertension.Scientific reports · 2023Article
- Improving Hereditary Hemorrhagic Telangiectasia Molecular Diagnosis: A Referral Center Experience.Genes · 2023Article
- Discovery of Highly Potent and BMPR2-Selective Kinase Inhibitors Using DNA-Encoded Chemical Library Screening.Journal of medicinal chemistry · 2023Article
13 more citing papers are in PubMed but not listed here.
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Authors and funding
2 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Rendu-Osler-Weber syndrome, also known as hereditary hemorrhagic telangiectasia (HHT), is an autosomal dominant vascular disorder. Three genes are causally related to HHT: the ENG gene encoding endoglin, a co-receptor of the TGFβ family (HHT1), the ACVRL1 gene encoding ALK1 (activin receptor-like kinase 1), a type I receptor of the TGFβ family (HHT2), and the SMAD4 gene, encoding a transcription factor critical for this signaling pathway. Bone morphogenetic proteins (BMPs) are growth factors of the TGFβ family. Among them, BMP9 and BMP10 have been shown to bind directly with high affinity to ALK1 and endoglin, and BMP9 mutations have recently been linked to a vascular anomaly syndrome that has phenotypic overlap with HHT. BMP9 and BMP10 are both circulating cytokines in blood, and the current working model is that BMP9 and BMP10 maintain a quiescent endothelial state that is dependent on the level of ALK1/endoglin activation in endothelial cells. In accordance with this model, to explain the etiology of HHT we hypothesize that a deficient BMP9/BMP10/ALK1/endoglin pathway may lead to re-activation of angiogenesis or a greater sensitivity to an angiogenic stimulus. Resulting endothelial hyperproliferation and hypermigration may lead to vasodilatation and generation of an arteriovenous malformation (AVM). HHT would thus result from a defect in the angiogenic balance. This review will focus on the emerging role played by BMP9 and BMP10 in the development of this disease and the therapeutic approaches that this opens.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.