Evidence map›Paper›PMID 27803996›Full record

ArticleJournal of molecular histology2017

CRIM1 is necessary for coronary vascular endothelial cell development and homeostasis.

Swati Iyer, Yash Chhabra, Tracey J Harvey, Richard Wang, Han Sheng Chiu, A G Smith, Walter G Thomas, David J Pennisi, Michael Piper

Abstract read
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In one paragraph

Article in Journal of molecular histology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
0.6field-weighted citation impact, top 29% 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

9 citing papers in PubMed, 12 citations in OpenAlex.

  1. Genetics-Informed Mapping Identifies a CRIM1-Associated Endocardial Inflammatory Remodeling State in Acute Myocardial Infarction.Medical science monitor : international medical journal of experimental and clinical research · 2026
    Article
  2. Review
  3. Article
  4. Article
  5. Article
  6. Essential Role of CRIM1 on Endometrial Receptivity in Goat.International journal of molecular sciences · 2021
    Article
  7. Article
  8. Review
  9. 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 1 institution in 1 country.

Swati IyerSchool of Biomedical Sciences, The University of Queensland, Brisbane, 4072, Australia.
Yash ChhabraSchool of Biomedical Sciences, The University of Queensland, Brisbane, 4072, Australia.
Tracey J HarveySchool of Biomedical Sciences, The University of Queensland, Brisbane, 4072, Australia.
Richard WangSchool of Biomedical Sciences, The University of Queensland, Brisbane, 4072, Australia.
Han Sheng ChiuSchool of Biomedical Sciences, The University of Queensland, Brisbane, 4072, Australia.
A G SmithSchool of Biomedical Sciences, The University of Queensland, Brisbane, 4072, Australia.
Walter G ThomasSchool of Biomedical Sciences, The University of Queensland, Brisbane, 4072, Australia.
David J PennisiSchool of Biomedical Sciences, The University of Queensland, Brisbane, 4072, Australia. d.pennisi@uq.edu.au.
Michael PiperSchool of Biomedical Sciences, The University of Queensland, Brisbane, 4072, Australia. m.piper@uq.edu.au.ORCID http://orcid.org/0000-0002-6759-2560
The University of Queensland · AU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Endothelial cells form a critical component of the coronary vasculature, yet the factors regulating their development remain poorly defined. Here we reveal a novel role for the transmembrane protein CRIM1 in mediating cardiac endothelial cell development. In the absence of Crim1 in vivo, the coronary vasculature is malformed, the number of endothelial cells reduced, and the canonical BMP pathway dysregulated. Moreover, we reveal that CRIM1 can bind IGFs, and regulate IGF signalling within endothelial cells. Finally, loss of CRIM1 from human cardiac endothelial cells results in misregulation of endothelial genes, predicted by pathway analysis to be involved in an increased inflammatory response and cytolysis, reminiscent of endothelial cell dysfunction in cardiovascular disease pathogenesis. Collectively, these findings implicate CRIM1 in endothelial cell development and homeostasis in the coronary vasculature.

Indexed as

HomeostasisAnimalsBone Morphogenetic Protein ReceptorsBone Morphogenetic ProteinsCell SurvivalCoronary VesselsEndothelial CellsHumansHuman Umbilical Vein Endothelial CellsMiceMice, KnockoutMutationSignal TransductionBone Morphogenetic Protein ReceptorsBone Morphogenetic ProteinsCrim1 protein, mouseCrim 1Endothelial cellsHeart

Identifiers

PMID27803996
OpenAlexW2548734591

What OpenQuestion holds

Textmetadata
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.