Evidence map›Paper›PMID 26778458›Full record

ReviewJournal of molecular and cellular cardiology2016

Extracellular matrix-mediated cellular communication in the heart.

Iñigo Valiente-Alandi, Allison E Schafer, Burns C Blaxall

Abstract readReview
In one paragraph

Review in Journal of molecular and cellular cardiology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 89 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
89citing papers in PubMed, 1 pooled it
13.7field-weighted citation impact, top 1% 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

89 citing papers in PubMed, 1 synthesis or guideline pooled it, 160 citations in OpenAlex.

  1. Pooled it
  2. Trial
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Advanced cardiac organoid model for studying doxorubicin-induced cardiotoxicity.Toxicological sciences : an official journal of the Society of Toxicology · 2025
    Article
  10. Article
  11. Review
  12. Article
  13. Review
  14. Article
  15. Review
  16. Tissue elasticity modulates cardiac pacemaker cell automaticity.American journal of physiology. Heart and circulatory physiology · 2025
    Article
  17. Review
  18. Article
  19. Review
  20. Review

29 more citing papers are in PubMed but not listed here.

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

3 authors at 1 institution in 1 country.

Iñigo Valiente-AlandiThe Heart Institute, Molecular Cardiovascular Biology, Cincinnati Children's Hospital Medical Center, Cincinnati, OH 45229, USA.
Allison E SchaferThe Heart Institute, Molecular Cardiovascular Biology, Cincinnati Children's Hospital Medical Center, Cincinnati, OH 45229, USA.
Burns C BlaxallThe Heart Institute, Molecular Cardiovascular Biology, Cincinnati Children's Hospital Medical Center, Cincinnati, OH 45229, USA. Electronic address: burns.blaxall@cchmc.org.
Cincinnati Children's Hospital Medical Center · US

Funding

WNT/^-catenin Signaling and Cardiac Fibrosis P01HL069779 · NHLBI · CINCINNATI CHILDRENS HOSP MED CTR · PI JAMES, JEANNE M · 2002 to 2017
$27.0M
Randomized clinical trial of sodium nitrite for out of hospital cardiac arrestR01HL129722 · NHLBI · UNIVERSITY OF WASHINGTON · PI KIM, FRANCIS · 2016 to 2020
$3.5M
Understanding Cardiovascular Disease MechanismsT32HL125204 · NHLBI · CINCINNATI CHILDRENS HOSP MED CTR · PI Evangelia G Kranias, Jeffery D Molkentin · 2015 to 2026
$3.4M
Targeting of B-AR/GBy signaling in the heart with small moleculesR01HL091475 · NHLBI · UNIVERSITY OF ROCHESTER · PI BLAXALL, BURNS C · 2010 to 2013
$1.5M
Small molecule targeting of MLK3 for heart failureR01HL129772 · NHLBI · CINCINNATI CHILDRENS HOSP MED CTR · PI BLAXALL, BURNS C · 2016 to 2018
$1.2M
Targeting fibronectin in cardiac remodeling and fibrosisR01HL134312 · NHLBI · CINCINNATI CHILDRENS HOSP MED CTR · PI BLAXALL, BURNS C · 2016 to 2018
$1.2M
NHLBI NIH HHS P01 HL069779NHLBI NIH HHS P01HL069779NHLBI NIH HHS R01 HL091475NHLBI NIH HHS R01HL091475NHLBI NIH HHS R01 HL129722NHLBI NIH HHS R01HL129722NHLBI NIH HHS R01 HL129772NHLBI NIH HHS R01 HL134312NHLBI NIH HHS T32 HL125204NHLBI NIH HHS T32HL125204
6 · The paper itself

Abstract

The extracellular matrix (ECM) is a complex and dynamic scaffold that maintains tissue structure and dynamics. However, the view of the ECM as an inert architectural support has been increasingly challenged. The ECM is a vibrant meshwork, a crucial organizer of cellular microenvironments. It plays a direct role in cellular interactions regulating cell growth, survival, spreading, proliferation, differentiation and migration through the intricate relationship among cellular and acellular tissue components. This complex interrelationship preserves cardiac function during homeostasis; however it is also responsible for pathologic remodeling following myocardial injury. Therefore, enhancing our understanding of this cross-talk may provide mechanistic insights into the pathogenesis of heart failure and suggest new approaches to novel, targeted pharmacologic therapies. This review explores the implications of ECM-cell interactions in myocardial cell behavior and cardiac function at baseline and following myocardial injury.

Indexed as

Cell Adhesion MoleculesCell CommunicationCollagenCytoskeletonExtracellular MatrixFibroblastsFibronectinsFibrosisGene Expression RegulationHeart FailureHeart InjuriesMyocardiumMyocytes, CardiacOsteonectinOsteopontinSignal TransductionCell Adhesion MoleculesCollagenFibronectinsOsteonectinOsteopontinPOSTN protein, humanSPARC protein, humanTenascinThrombospondinsCardiac remodelingExtracellular matrixFibroblastFibrosis

Identifiers

PMID26778458
PMCPMC4767504
OpenAlexW2239366382

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.