Evidence map›Paper›PMID 32762495›Full record

ArticleCirculation research2020

Overexpression of Activin Receptor-Like Kinase 1 in Endothelial Cells Suppresses Development of Arteriovenous Malformations in Mouse Models of Hereditary Hemorrhagic Telangiectasia.

Yong Hwan Kim, Phuong-Nhung Vu, Se-Woon Choe, Chang-Jin Jeon, Helen M Arthur, Calvin P H Vary, Young Jae Lee, S Paul Oh

Open access · bronzeAbstract read
In one paragraph

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 39 papers.

0numbers the graph read from it
0cells of the map it votes in
39citing papers in PubMed
3.9field-weighted citation impact, top 6% 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

39 citing papers in PubMed, 57 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Bone morphogenetic protein-9 controls pulmonary vascular growth and remodeling.Proceedings of the National Academy of Sciences of the United States of America · 2025
    Article
  5. Review
  6. Article
  7. Hereditary haemorrhagic telangiectasia.Nature reviews. Disease primers · 2025
    Review
  8. Review
  9. Review
  10. Review
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Review
  18. Blood flow regulatesbioRxiv : the preprint server for biology · 2024
    Article
  19. Review
  20. Review
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

8 authors at 6 institutions in 3 countries.

Yong Hwan KimDepartment of Physiology and Functional Genomics, College of Medicine, University of Florida, Gainesville (Y.H.K., S.-w.C., S.P.O.).
Phuong-Nhung VuLee Gil Ya Cancer and Diabetes Institute, Gachon University, Incheon, Republic of Korea (N.V.P., Y.J.L.).
Se-Woon ChoeDepartment of Physiology and Functional Genomics, College of Medicine, University of Florida, Gainesville (Y.H.K., S.-w.C., S.P.O.).
Chang-Jin JeonDepartment of Biology, College of Natural Sciences, Kyungpook National University, Daegu, Korea (C.J.J.).
Helen M ArthurInstitute of Genetic Medicine, Newcastle University, United Kingdom (H.M.A.).
Calvin P H VaryCenter for Molecular Medicine, Maine Medical Center Research Institute, Scarborough (C.P.V.).
Young Jae LeeLee Gil Ya Cancer and Diabetes Institute, Gachon University, Incheon, Republic of Korea (N.V.P., Y.J.L.).
S Paul OhDepartment of Physiology and Functional Genomics, College of Medicine, University of Florida, Gainesville (Y.H.K., S.-w.C., S.P.O.).
Barrow Neurological Institute · USGachon University · KRKumoh National Institute of Technology · KRKyungpook National University · KRMaine Medical Center · USNewcastle University · GB

Funding

Molecular determinants of the fate of human heart mesenchymal progenitor cellsR01HL139887 · NHLBI · MAINEHEALTH · PI SAWYER, DOUGLAS B, VARY, CALVIN PARDEE HULL · 2019 to 2022
$2.0M
ROLE OF MACROPHAGES IN HHT PATHOGENESIS AND THERAPYR01HL128525 · NHLBI · UNIVERSITY OF FLORIDA · PI OH, SUK PAUL · 2015 to 2018
$1.6M
British Heart Foundation PG/14/86/31177British Heart Foundation PG/18/57/33941NHLBI NIH HHS R01 HL128525NHLBI NIH HHS R01 HL139887
6 · The paper itself

Abstract

rationaleHereditary hemorrhagic telangiectasia (HHT) is a genetic disease caused by mutations in

objectiveWe tested this hypothesis and investigated the therapeutic effects and potential risks of induced-ALK1 or -ENG overexpression (OE) for HHT. METHODS AND

resultsWe generated a novel mouse allele (ROSA26

conclusionsThese data support the notion that ENG and ALK1 form a linear signaling pathway for the formation of a proper arteriovenous network during angiogenesis. We suggest that ALK1 OE or activation can be an effective therapeutic strategy for HHT. Further research is required to study whether this therapy could be translated into treatment for humans.

Indexed as

Activin Receptors, Type IIAllelesAnimalsApoptosis Regulatory ProteinsArteriovenous MalformationsDisease Models, AnimalEndoglinEndothelial CellsGreen Fluorescent ProteinsGrowth Differentiation Factor 2MiceMitochondrial ProteinsReceptors, NotchRetinal VesselsRNA, UntranslatedSignal TransductionActivin Receptors, Type IIAcvrl1 protein, mouseApoptosis Regulatory ProteinsDiablo protein, mouseEndoglinEng protein, mouseenhanced green fluorescent proteinGreen Fluorescent ProteinsGrowth Differentiation Factor 2Gt(ROSA)26Sor non-coding RNA, mouseMitochondrial ProteinsReceptors, NotchRNA, UntranslatedSmad4 ProteinSmad4 protein, mouseTransforming Growth Factor betaactivin receptor-like kinase 1arteriovenous malformationendoglinendothelial cellhereditary hemorrhagic telangiectasiamicesignal transduction

Identifiers

PMID32762495
PMCPMC7554133
OpenAlexW3046695108

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.