ReviewGenes2021
Hereditary Haemorrhagic Telangiectasia, an Inherited Vascular Disorder in Need of Improved Evidence-Based Pharmaceutical Interventions.
Review in Genes, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
29 citing papers in PubMed, 51 citations in OpenAlex.
- Targeting KIT prevents brain arteriovenous malformations driven by ALK1-deficient angiogenic endothelial cells.The Journal of clinical investigation · 2026Article
- A microphysiological system HHT-on-a-chip platform recapitulates patient vascular lesions.Nature communications · 2026Article
- Endovascular Embolization in Neurovascular Disease: Material Science, Multimodal Management, and Future Horizons.Biomedicines · 2026Review
- Modeling Somatic Second-Hit Mutations in Novel Mouse Models of Hereditary Hemorrhagic Telangiectasia.bioRxiv : the preprint server for biology · 2026Article
- Vascular endothelial generating factor pathway in ovarian cancer.Journal of ovarian research · 2025Review
- Common and distinct circulating microRNAs in four neurovascular disorders.Biochemistry and biophysics reports · 2025Article
- Hereditary haemorrhagic telangiectasia.Nature reviews. Disease primers · 2025Review
- Association of Plasma Inflammatory Proteins and Intracerebral Hemorrhage in Pediatric Brain Arteriovenous Malformations.Pediatric stroke · 2025Article
- The role of endothelial cell-pericyte interactions in vascularization and diseases.Journal of advanced research · 2025Review
- Diagnostic and Prognostic Value of Angiogenic Status in Hereditary Hemorrhagic Telangiectasia.Diagnostics (Basel, Switzerland) · 2024Article
- Medical and Interventional Management of Hereditary Hemorrhagic Telangiectasia.Seminars in interventional radiology · 2024Review
- Article
- Hereditary hemorrhagic telangiectasia: from signaling insights to therapeutic advances.The Journal of clinical investigation · 2024Review
- Specifications of the ACMG/AMP Variant Curation Guidelines for Hereditary Hemorrhagic Telangiectasia Genes-Human mutation · 2024Article
- Therapeutic targeting of vascular malformation in a zebrafish model of hereditary haemorrhagic telangiectasia.Disease models & mechanisms · 2023Article
- BMP10 functions independently from BMP9 for the development of a proper arteriovenous network.Angiogenesis · 2023Article
- Oxidative stress-induced MMP- and γ-secretase-dependent VE-cadherin processing is modulated by the proteasome and BMP9/10.Scientific reports · 2023Article
- Pericytes and vascular smooth muscle cells in central nervous system arteriovenous malformations.Frontiers in physiology · 2023Review
- Pulmonary Arteriovenous Malformation in a Rare Case of Hereditary Hemorrhagic Telangiectasia.Cureus · 2022Article
- Environmental and intrinsic modulations of venous differentiation.Cellular and molecular life sciences : CMLS · 2022Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
Hereditary haemorrhagic telangiectasia (HHT) is characterised by arteriovenous malformations (AVMs). These vascular abnormalities form when arteries and veins directly connect, bypassing the local capillary system. Large AVMs may occur in the lungs, liver and brain, increasing the risk of morbidity and mortality. Smaller AVMs, known as telangiectases, are prevalent on the skin and mucosal lining of the nose, mouth and gastrointestinal tract and are prone to haemorrhage. HHT is primarily associated with a reduction in endoglin (ENG) or ACVRL1 activity due to loss-of-function mutations. ENG and ACVRL1 transmembrane receptors are expressed on endothelial cells (ECs) and bind to circulating ligands BMP9 and BMP10 with high affinity. Ligand binding to the receptor complex leads to activation of the SMAD1/5/8 signalling pathway to regulate downstream gene expression. Various genetic animal models demonstrate that disruption of this pathway in ECs results in AVMs. The vascular abnormalities underlying AVM formation result from abnormal EC responses to angiogenic and haemodynamic cues, and include increased proliferation, reduced migration against the direction of blood flow and an increased EC footprint. There is growing evidence that targeting VEGF signalling has beneficial outcomes in HHT patients and in animal models of this disease. The anti-VEGF inhibitor bevacizumab reduces epistaxis and has a normalising effect on high cardiac output in HHT patients with hepatic AVMs. Blocking VEGF signalling also reduces vascular malformations in mouse models of HHT1 and HHT2. However, VEGF signalling is complex and drives numerous downstream pathways, and it is not yet clear which pathway (or combination of pathways) is critical to target. This review will consider the recent evidence gained from HHT clinical and preclinical studies that are increasing our understanding of HHT pathobiology and informing therapeutic strategies.
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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.