Evidence map›Paper›PMID 31958058›Full record

ArticleeLife2020

YAP1 and TAZ negatively control bone angiogenesis by limiting hypoxia-inducible factor signaling in endothelial cells.

Kishor K Sivaraj, Backialakshmi Dharmalingam, Vishal Mohanakrishnan, Hyun-Woo Jeong, Katsuhiro Kato, Silke Schröder, Susanne Adams, Gou Young Koh, Ralf H Adams

Open access · goldAbstract read
In one paragraph

Article in eLife, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 papers.

0numbers the graph read from it
0cells of the map it votes in
49citing papers in PubMed
5.7field-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

49 citing papers in PubMed, 98 citations in OpenAlex.

  1. Review
  2. Angiogenesis in Lung Regeneration and Aging.Arteriosclerosis, thrombosis, and vascular biology · 2026
    Review
  3. Article
  4. Review
  5. Review
  6. Article
  7. Article
  8. Review
  9. Article
  10. Article
  11. Article
  12. Review
  13. Review
  14. Article
  15. Article
  16. Article
  17. Regulation of YAP Promotor Accessibility in Endothelial Mechanotransduction.Arteriosclerosis, thrombosis, and vascular biology · 2024
    Article
  18. Targeting type H vessels in bone-related diseases.Journal of cellular and molecular medicine · 2024
    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

9 authors at 2 institutions in 2 countries.

Kishor K SivarajDepartment of Tissue Morphogenesis, Max Planck Institute for Molecular Biomedicine, Münster, Germany.ORCID 0000-0002-5321-3400
Backialakshmi DharmalingamDepartment of Tissue Morphogenesis, Max Planck Institute for Molecular Biomedicine, Münster, Germany.
Vishal MohanakrishnanDepartment of Tissue Morphogenesis, Max Planck Institute for Molecular Biomedicine, Münster, Germany.
Hyun-Woo JeongDepartment of Tissue Morphogenesis, Max Planck Institute for Molecular Biomedicine, Münster, Germany.
Katsuhiro KatoDepartment of Tissue Morphogenesis, Max Planck Institute for Molecular Biomedicine, Münster, Germany.
Silke SchröderDepartment of Tissue Morphogenesis, Max Planck Institute for Molecular Biomedicine, Münster, Germany.
Susanne AdamsDepartment of Tissue Morphogenesis, Max Planck Institute for Molecular Biomedicine, Münster, Germany.
Gou Young KohCenter for Vascular Research, Institute of Basic Science (IBS), Daejeon, Republic of Korea.
Ralf H AdamsDepartment of Tissue Morphogenesis, Max Planck Institute for Molecular Biomedicine, Münster, Germany.ORCID 0000-0003-3031-7677
University of Münster · DEKorea Advanced Institute of Science and Technology · KR

Funding

H2020 European Research Council AdG 786672 PROVECMax-Planck-Gesellschaft Open-access funding
6 · The paper itself

Abstract

Blood vessels are integrated into different organ environments with distinct properties and physiology (Augustin and Koh, 2017). A striking example of organ-specific specialization is the bone vasculature where certain molecular signals yield the opposite effect as in other tissues (Glomski et al., 2011; Kusumbe et al., 2014; Ramasamy et al., 2014). Here, we show that the transcriptional coregulators Yap1 and Taz, components of the Hippo pathway, suppress vascular growth in the hypoxic microenvironment of bone, in contrast to their pro-angiogenic role in other organs. Likewise, the kinase Lats2, which limits Yap1/Taz activity, is essential for bone angiogenesis but dispensable in organs with lower levels of hypoxia. With mouse genetics, RNA sequencing, biochemistry, and cell culture experiments, we show that Yap1/Taz constrain hypoxia-inducible factor 1α (HIF1α) target gene expression in vivo and in vitro. We propose that crosstalk between Yap1/Taz and HIF1α controls angiogenesis depending on the level of tissue hypoxia, resulting in organ-specific biological responses.

Indexed as

Adaptor Proteins, Signal TransducingAnimalsCell Cycle ProteinsCell HypoxiaEndothelial CellsHippo Signaling PathwayHypoxia-Inducible Factor 1, alpha SubunitMaleMiceMice, Inbred C57BLNeovascularization, PhysiologicOsteogenesisProtein Serine-Threonine KinasesSignal TransductionTrans-ActivatorsYAP-Signaling ProteinsAdaptor Proteins, Signal TransducingCell Cycle ProteinsHif1a protein, mouseHypoxia-Inducible Factor 1, alpha SubunitProtein Serine-Threonine KinasesTrans-ActivatorsWwtr1 protein, mouseYap1 protein, mouseYAP-Signaling Proteinsangiogenesisbonecell biologydevelopmental biologyendothelial cellsHippo signalinghypoxiamouse

Identifiers

PMID31958058
PMCPMC6970532
OpenAlexW2999619546

What OpenQuestion holds

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LicenceCC BY
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.