Evidence map›Paper›PMID 31828546›Full record

ArticleAngiogenesis2020

BMP10-mediated ALK1 signaling is continuously required for vascular development and maintenance.

Teresa L Capasso, Bijun Li, Harry J Volek, Waqas Khalid, Elizabeth R Rochon, Arulselvi Anbalagan, Chelsea Herdman, H Joseph Yost, Flordeliza S Villanueva, Kang Kim and 1 more

Open access · greenAbstract read
In one paragraph

Article in Angiogenesis, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 59 papers.

0numbers the graph read from it
0cells of the map it votes in
59citing papers in PubMed
5.8field-weighted citation impact, top 3% of its field
1 · What the graph read from it

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

59 citing papers in PubMed, 77 citations in OpenAlex.

  1. Article
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  5. Discovery ofDiagnostics (Basel, Switzerland) · 2025
    Article
  6. Review
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  8. Prodomain processing controls BMP-10 bioactivity and targeting to fibrillin-1 in latent conformation.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2025
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  9. Review
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  18. Blood flow regulatesbioRxiv : the preprint server for biology · 2024
    Article
  19. Article
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

11 authors at 2 institutions in 1 country.

Teresa L CapassoDepartment of Human Genetics, Graduate School of Public Health, University of Pittsburgh, Pittsburgh, PA, 15261, USA.
Bijun LiDepartment of Human Genetics, Graduate School of Public Health, University of Pittsburgh, Pittsburgh, PA, 15261, USA.
Harry J VolekDepartment of Bioengineering, Swanson School of Engineering, University of Pittsburgh, Pittsburgh, PA, 15260, USA.
Waqas KhalidDepartment of Bioengineering, Swanson School of Engineering, University of Pittsburgh, Pittsburgh, PA, 15260, USA.
Elizabeth R RochonDepartment of Human Genetics, Graduate School of Public Health, University of Pittsburgh, Pittsburgh, PA, 15261, USA.
Arulselvi AnbalaganDepartment of Human Genetics, Graduate School of Public Health, University of Pittsburgh, Pittsburgh, PA, 15261, USA.
Chelsea HerdmanMolecular Medicine Program, University of Utah, Salt Lake City, UT, 84112, USA.
H Joseph YostMolecular Medicine Program, University of Utah, Salt Lake City, UT, 84112, USA.
Flordeliza S VillanuevaHeart, Lung, Blood and Vascular Medicine Institute, University of Pittsburgh, Pittsburgh, PA, 15261, USA.
Kang KimDepartment of Bioengineering, Swanson School of Engineering, University of Pittsburgh, Pittsburgh, PA, 15260, USA.
Beth L RomanDepartment of Human Genetics, Graduate School of Public Health, University of Pittsburgh, Pittsburgh, PA, 15261, USA. romanb@pitt.edu.ORCID 0000-0002-1250-1705
University of Pittsburgh · USUniversity of Utah · US

Funding

ADVANCING ZINC FINGER NUCLEASES FOR TARGETED GENOME MANIPULATIONR01GM088040 · NIGMS · MASSACHUSETTS GENERAL HOSPITAL · PI JOUNG, J. KEITH, PETERSON, RANDALL T · 2009 to 2016
$4.5M
Genome-Wide Analysis of Cardiac Development in ZebrafishUM1HL098160 · NHLBI · UNIVERSITY OF UTAH · PI YOST, H. JOSEPH · 2015 to 2019
$3.7M
Interaction between blood flow and ALK1 signaling in AVM developmentR01HL136566 · NHLBI · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI ROMAN, BETH L · 2017 to 2020
$1.7M
BMP10 IN CARDIOVASCULAR DEVELOPMENT AND HEREDITARY HEMORRHAGIC TELANGIECTASIAR01HL133009 · NHLBI · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI ROMAN, BETH L · 2016 to 2019
$1.6M
High-resolution ultrasound in-vivo animal imaging system-Vevo2100S10RR027383 · NCRR · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI KIM, KANG · 2010 to 2010
$498k
NCRR NIH HHS S10 RR027383NHLBI NIH HHS R01 HL133009NHLBI NIH HHS R01 HL136566NHLBI NIH HHS UM1 HL098160NIGMS NIH HHS R01 GM088040
6 · The paper itself

Abstract

Hereditary hemorrhagic telangiectasia (HHT) is an autosomal-dominant vascular disorder characterized by development of high-flow arteriovenous malformations (AVMs) that can lead to stroke or high-output heart failure. HHT2 is caused by heterozygous mutations in ACVRL1, which encodes an endothelial cell bone morphogenetic protein (BMP) receptor, ALK1. BMP9 and BMP10 are established ALK1 ligands. However, the unique and overlapping roles of these ligands remain poorly understood. To define the physiologically relevant ALK1 ligand(s) required for vascular development and maintenance, we generated zebrafish harboring mutations in bmp9 and duplicate BMP10 paralogs, bmp10 and bmp10-like. bmp9 mutants survive to adulthood with no overt phenotype. In contrast, combined loss of bmp10 and bmp10-like results in embryonic lethal cranial AVMs indistinguishable from acvrl1 mutants. However, despite embryonic functional redundancy of bmp10 and bmp10-like, bmp10 encodes the only required Alk1 ligand in the juvenile-to-adult period. bmp10 mutants exhibit blood vessel abnormalities in anterior skin and liver, heart dysmorphology, and premature death, and vascular defects correlate with increased cardiac output. Together, our findings support a unique role for Bmp10 as a non-redundant Alk1 ligand required to maintain the post-embryonic vasculature and establish zebrafish bmp10 mutants as a model for AVM-associated high-output heart failure, which is an increasingly recognized complication of severe liver involvement in HHT2.

Indexed as

Activin ReceptorsAnimalsAnimals, Genetically ModifiedArteriovenous MalformationsBlood VesselsBone Morphogenetic ProteinsCell DifferentiationEmbryo, NonmammalianEndothelial CellsGene Expression Regulation, DevelopmentalNeovascularization, PhysiologicRegenerationSignal TransductionZebrafishZebrafish ProteinsActivin ReceptorsAcvrl1 protein, zebrafishbmp10 protein, zebrafishBone Morphogenetic ProteinsZebrafish ProteinsBone morphogenetic proteinHereditary hemorrhagic telangiectasiaVascular developmentZebrafish

Identifiers

PMID31828546
PMCPMC7165044
OpenAlexW2996287339

What OpenQuestion holds

Textmetadata
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Read underepoch 390

Registered trials

None linked

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.