Evidence map›Paper›PMID 26906028›Full record

ReviewCurrent opinion in hematology2016

Pulling on my heartstrings: mechanotransduction in cardiac development and function.

Margaret E McCormick, Ellie Tzima

Open access · greenAbstract readReview
In one paragraph

Review in Current opinion in hematology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
1.3field-weighted citation impact, top 18% 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

11 citing papers in PubMed, 16 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Review
  5. Article
  6. Article
  7. Contractility of Induced Pluripotent Stem Cell-Cardiomyocytes With anFrontiers in cell and developmental biology · 2020
    Article
  8. Review
  9. Article
  10. Article
  11. 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 2 countries.

Margaret E McCormickaInstitute for Medicine and Engineering bDepartment of Pathology and Laboratory Medicine, Perelman School of Medicine, University of Pennsylvania, Philadelphia, Pennsylvania, USA cDivision of Cardiovascular Medicine, Wellcome Trust Centre for Human Genetics, Oxford University, Oxford, UK.
Ellie Tzima
University of Oxford · GB

Funding

Multidisciplinary Training in Cardiovascular BiologyT32HL007954 · NHLBI · UNIVERSITY OF PENNSYLVANIA · PI DAVIES, PETER FRANCIS · 2000 to 2019
$9.9M
Mechanisms of neovascularization in response to ischemiaR01HL117256 · NHLBI · UNIV OF NORTH CAROLINA CHAPEL HILL · PI BAUTCH, VICTORIA L · 2014 to 2017
$1.5M
NHLBI NIH HHS HL117256NHLBI NIH HHS R01 HL117256NHLBI NIH HHS T32 HL007954NHLBI NIH HHS T32 HL07954Wellcome Trust
6 · The paper itself

Abstract

purpose of reviewEndothelial cells line the surface of the cardiovascular system and display a large degree of heterogeneity due to developmental origin and location. Despite this heterogeneity, all endothelial cells are exposed to wall shear stress (WSS) imparted by the frictional force of flowing blood, which plays an important role in determining the endothelial cell phenotype. Although the effects of WSS have been greatly studied in vascular endothelial cells, less is known about the role of WSS in regulating cardiac function and cardiac endothelial cells. RECENT

findingsRecent advances in genetic and imaging technologies have enabled a more thorough investigation of cardiac hemodynamics. Using developmental models, shear stress sensing by endocardial endothelial cells has been shown to play an integral role in proper cardiac development including morphogenesis and formation of the conduction system. In the adult, less is known about hemodynamics and endocardial endothelial cells, but a clear role for WSS in the development of coronary and valvular disease is increasingly appreciated. SUMMARY: Future research will further elucidate a role for WSS in the developing and adult heart, and understanding this dynamic relationship may represent a potential therapeutic target for the treatment of cardiomyopathies.

Indexed as

Mechanotransduction, CellularCardiovascular SystemEndothelial CellsHemodynamicsHumansStress, Mechanical

Identifiers

PMID26906028
PMCPMC4823169
OpenAlexW2324131865

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.