ArticleCirculation research2020
Loss of Endothelial Endoglin Promotes High-Output Heart Failure Through Peripheral Arteriovenous Shunting Driven by VEGF Signaling.
Article in Circulation research, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
48 citing papers in PubMed, 69 citations in OpenAlex.
- SGLT2 inhibitor therapy is associated with IL-10/TGF-α/sVEGFR3 signalling and adipose tissue remodelling in advanced heart failure.Journal of molecular and cellular cardiology plus · 2026Article
- Lung Pericytes: Molecular Mechanisms, Signaling Pathways, and Roles in Pulmonary Diseases.Comprehensive Physiology · 2026Review
- Live imaging of vascular dynamics in mouse skin.The Journal of investigative dermatology · 2026Article
- Modeling Somatic Second-Hit Mutations in Novel Mouse Models of Hereditary Hemorrhagic Telangiectasia.bioRxiv : the preprint server for biology · 2026Article
- Non-invasive characterization of pericyte dysfunction in mouse brain using functional ultrasound localization microscopy.Nature biomedical engineering · 2026Article
- Endoglin as a BMP9 co-receptor in vascular endothelial cells: prodomain displacement and TGFBRII recruitment.Nature communications · 2025Article
- Integrated trajectories of systolic and diastolic function differentially associate with risk for heart failure with preserved and reduced ejection fraction and proteomic profiles.European journal of heart failure · 2025Article
- Arteriovenous Malformations (AVMs): Molecular Pathogenesis, Clinical Features, and Emerging Therapeutic Strategies.Biomolecules · 2025Review
- ALK1-BMPRII agonism by clustering bispecific antibodies treats hereditary hemorrhagic telangiectasia.bioRxiv : the preprint server for biology · 2025Article
- Mouse model of post-traumatic stress disorder negatively impacts cardiac homeostasis.Journal of molecular and cellular cardiology · 2025Article
- From bench to bedside: murine models of inherited and sporadic brain arteriovenous malformations.Angiogenesis · 2025Review
- GenX induces offspring vascular endothelial ferroptosis by targeting GPX4 for ubiquitination-dependent degradation.Current research in toxicology · 2025Article
- Genetic and pharmacological targeting of mTORC1 in mouse models of arteriovenous malformation expose non-cell autonomous signalling in HHT.Angiogenesis · 2024Article
- Activins and Inhibins in Cardiovascular Pathophysiology.Biomolecules · 2024Review
- Ancestrally diverse genome-wide association analysis highlights ancestry-specific differences in genetic regulation of plasma protein levels.medRxiv : the preprint server for health sciences · 2024Article
- Thyroid Arteriovenous Malformation in Hereditary Hemorrhagic Telangiectasia: Insights on Successful Noninvasive Imaging.JCEM case reports · 2024Article
- Medical and Interventional Management of Hereditary Hemorrhagic Telangiectasia.Seminars in interventional radiology · 2024Review
- Increasing Endoglin Deletion in Endothelial Cells Exacerbates the Severity of Brain Arteriovenous Malformation in Mouse.Biomedicines · 2024Article
- Novel radiopaque ethanol injection: physicochemical properties, animal experiments, and clinical application in vascular malformations.Military Medical Research · 2024Article
- Shear stress and pathophysiological PI3K involvement in vascular malformations.The Journal of clinical investigation · 2024Review
Corrections and comments
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Authors and funding
13 authors at 2 institutions in 2 countries.
Funding
Abstract
rationaleENG (endoglin) is a coreceptor for BMP (bone morphogenetic protein) 9/10 and is strongly expressed in endothelial cells. Mutations in
objectiveThe goal of the work was to determine how ENG maintains vessel caliber in adult life to prevent AVM formation and thereby protect heart function. METHODS AND
resultsGenetic depletion of endothelial
conclusionsENG promotes the normal balance of VEGF signaling in quiescent endothelial cells to maintain vessel caliber-an essential function in conditions of increased VEGF expression such as local hypoxia or inflammation. In the absence of endothelial ENG, increased sensitivity to VEGF drives abnormal endothelial proliferation in local regions of high VEGF expression, leading to AVM formation and a rapid injurious impact on heart function.
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What OpenQuestion holds
Registered trials
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.