Evidence map›Paper›PMID 28871312›Full record

ReviewCellular and molecular life sciences : CMLS2017

ALK1 signaling in development and disease: new paradigms.

Beth L Roman, Andrew P Hinck

Open access · greenAbstract readReview
In one paragraph

Review in Cellular and molecular life sciences : CMLS, 2017. 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
6.0field-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, 105 citations in OpenAlex.

  1. Article
  2. Tumor-Induced PDPNInternational journal of molecular sciences · 2026
    Article
  3. Review
  4. Review
  5. Article
  6. Article
  7. Review
  8. Article
  9. 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
    Article
  10. Review
  11. Article
  12. Hereditary haemorrhagic telangiectasia.Nature reviews. Disease primers · 2025
    Review
  13. Review
  14. Article
  15. Article
  16. Review
  17. Article
  18. Review
  19. Article
  20. Article
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

2 authors at 1 institution in 1 country.

Beth L RomanDepartment of Human Genetics, University of Pittsburgh Graduate School of Public Health, 130 DeSoto St, Pittsburgh, PA, 15261, USA. romanb@pitt.edu.
Andrew P HinckDepartment of Structural Biology, University of Pittsburgh School of Medicine, Pittsburgh, PA, USA.
University of Pittsburgh · US

Funding

TISSUE CULTURE---COREP30CA054174 · NCI · UNIVERSITY OF TEXAS HLTH SCIENCE CENTER · PI Robin Jean Leach · 1991 to 2026
$59.1M
LIGAND/RECEPTOR INTERACTIONS IN THE TGF BETA SUPERFAMILYR01GM058670 · NIGMS · UNIVERSITY OF TEXAS HLTH SCIENCE CENTER · PI HINCK, ANDREW P · 1999 to 2017
$3.6M
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
NCI NIH HHS P30 CA054174NHLBI NIH HHS R01 HL133009NHLBI NIH HHS R01 HL136566NIGMS NIH HHS R01 GM058670
6 · The paper itself

Abstract

Activin A receptor like type 1 (ALK1) is a transmembrane serine/threonine receptor kinase in the transforming growth factor-beta receptor family that is expressed on endothelial cells. Defects in ALK1 signaling cause the autosomal dominant vascular disorder, hereditary hemorrhagic telangiectasia (HHT), which is characterized by development of direct connections between arteries and veins, or arteriovenous malformations (AVMs). Although previous studies have implicated ALK1 in various aspects of sprouting angiogenesis, including tip/stalk cell selection, migration, and proliferation, recent work suggests an intriguing role for ALK1 in transducing a flow-based signal that governs directed endothelial cell migration within patent, perfused vessels. In this review, we present an updated view of the mechanism of ALK1 signaling, put forth a unified hypothesis to explain the cellular missteps that lead to AVMs associated with ALK1 deficiency, and discuss emerging roles for ALK1 signaling in diseases beyond HHT.

Indexed as

Activin Receptors, Type IIAnimalsEndothelial CellsHumansReceptors, Transforming Growth Factor betaSignal TransductionTelangiectasia, Hereditary HemorrhagicActivin Receptors, Type IIReceptors, Transforming Growth Factor betaActivin A receptor like type 1AngiogenesisArteriovenous malformationBone morphogenetic proteinEndoglinHereditary hemorrhagic telangiectasia

Identifiers

PMID28871312
PMCPMC5687069
OpenAlexW2750798761

What OpenQuestion holds

Textmetadata
LicenceTDM
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.