Evidence map›Paper›PMID 26562414›Full record

ReviewJournal of molecular and cellular cardiology2016

Integrins and integrin-related proteins in cardiac fibrosis.

Chao Chen, Ruixia Li, Robert S Ross, Ana Maria Manso

Open access · greenAbstract 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 95 papers.

0numbers the graph read from it
0cells of the map it votes in
95citing papers in PubMed
6.3field-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

95 citing papers in PubMed, 157 citations in OpenAlex.

  1. Review
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  10. Novel Drug Targets in Diastolic Heart Disease.International journal of molecular sciences · 2025
    Review
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35 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

4 authors at 1 institution in 1 country.

Chao ChenDepartment of Medicine, Cardiology, UCSD School of Medicine, La Jolla, CA 92093-0613, USA; Veterans Administration San Diego Healthcare System, San Diego, CA 92161, USA. Electronic address: chaochen@ucsd.edu.
Ruixia LiDepartment of Medicine, Cardiology, UCSD School of Medicine, La Jolla, CA 92093-0613, USA; Veterans Administration San Diego Healthcare System, San Diego, CA 92161, USA. Electronic address: rli@ucsd.edu.
Robert S RossDepartment of Medicine, Cardiology, UCSD School of Medicine, La Jolla, CA 92093-0613, USA; Veterans Administration San Diego Healthcare System, San Diego, CA 92161, USA. Electronic address: rross@ucsd.edu.
Ana Maria MansoDepartment of Medicine, Cardiology, UCSD School of Medicine, La Jolla, CA 92093-0613, USA; Veterans Administration San Diego Healthcare System, San Diego, CA 92161, USA. Electronic address: amanso@ucsd.edu.
UC San Diego Health System · US

Funding

Vector Production CoreP01HL066941 · NHLBI · VETERANS MEDICAL RESEARCH FDN/SAN DIEGO · PI FARQUHAR, MARILYN GIST · 2001 to 2017
$34.8M
Integrins and Caveolin Proteins in Cardiac Hypertrophy and FailureR01HL115933 · NHLBI · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI ROSS, ROBERT SCOTT, ROTH, DAVID M · 2013 to 2016
$2.6M
Cardiomyocyte mechanotransduction through the integrin complexR01HL103566 · NHLBI · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI OMENS, JEFFREY H., ROSS, ROBERT SCOTT · 2010 to 2014
$1.9M
Cardiac Myocyte Form and Function: Role of Talin and KindlinR01HL127806 · NHLBI · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI ROSS, ROBERT SCOTT · 2015 to 2018
$1.6M
NHLBI NIH HHS P01 HL066941NHLBI NIH HHS R01 HL103566NHLBI NIH HHS R01 HL115933NHLBI NIH HHS R01 HL127806
6 · The paper itself

Abstract

Cardiac fibrosis is one of the major components of the healing mechanism following any injury of the heart and as such may contribute to both systolic and diastolic dysfunction in a range of pathophysiologic conditions. Canonically, it can occur as part of the remodeling process that occurs following myocardial infarction or that follows as a response to pressure overload. Integrins are cell surface receptors which act in both cellular adhesion and signaling. Most importantly, in the context of the continuously contracting myocardium, they are recognized as mechanotransducers. They have been implicated in the development of fibrosis in several organs, including the heart. This review will focus on the involvement of integrins and integrin-related proteins, in cardiac fibrosis, outlining the roles of these proteins in the fibrotic responses in specific cardiac pathologies, discuss some of the common end effectors (angiotensin II, transforming growth factor beta 1 and mechanical stress) through which integrins function and finally discuss how manipulation of this set of proteins may lead to new treatments which could prove useful to alter the deleterious effects of cardiac fibrosis.

Indexed as

Age FactorsAgingAngiotensin IIAnimalsBlood PressureCarrier ProteinsCytokinesDiabetic CardiomyopathiesEpithelial-Mesenchymal TransitionFibrosisHumansIntegrinsMolecular Targeted TherapyMyocardial InfarctionMyocardiumProtein BindingAngiotensin IICarrier ProteinsCytokinesIntegrinsAngiotensinFibrosisIntegrinsMechanical stressMyocardiumTransforming growth factor beta

Identifiers

PMID26562414
PMCPMC4846493
OpenAlexW2180493842

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.