Evidence map›Paper›PMID 20093048›Full record

ArticleCardiovascular pathology : the official journal of the Society for Cardiovascular Pathology

Remodeling of cardiac fibroblasts following myocardial infarction results in increased gap junction intercellular communication.

Yan Zhang, Evelyn M Kanter, Kathryn A Yamada

Open access · greenAbstract read
In one paragraph

Article in Cardiovascular pathology : the official journal of the Society for Cardiovascular Pathology. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
37citing papers in PubMed, 1 pooled it
2.4field-weighted citation impact, top 11% 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

37 citing papers in PubMed, 1 synthesis or guideline pooled it, 67 citations in OpenAlex.

  1. Pooled it
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  17. The diagnostic value of circulating microRNAs in heart failure.Experimental and therapeutic medicine · 2019
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  20. GAmerican journal of physiology. Heart and circulatory physiology · 2017
    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

3 authors at 1 institution in 1 country.

Yan ZhangDepartment of Medicine (Cardiovascular Division and the Center for Cardiovascular Research), Washington University School of Medicine, St. Louis, MO, USA.
Evelyn M Kanter
Kathryn A Yamada
Washington University in St. Louis · US

Funding

STRUCTURAL &ELECTRICAL REMODELING OF CARDIAC CONNEXIN45R01HL066350 · NHLBI · WASHINGTON UNIVERSITY · PI YAMADA, KATHRYN A · 2000 to 2008
$2.9M
ANIMAL SUPPORT SPACE FOR NEUROSCIENCEC06RR015502 · NCRR · WASHINGTON UNIVERSITY · PI CICERO, THEODORE J · 2000 to 2000
$2.0M
NCRR NIH HHS C06 RR015502NHLBI NIH HHS HL066350NHLBI NIH HHS R01 HL066350
6 · The paper itself

Abstract

backgroundWe have recently shown that native murine ventricular fibroblasts express both connexin43 (Cx43) and Cx45, and that the level of Cx43 expression influences intercellular coupling and cell proliferation. Relatively little is known, however, about how myocardial infarction (MI) influences expression of Cx43, or how altered Cx43 expression may affect fibroblast function post-MI. Fibroblasts are critical for infarct healing and post-infarct ventricular remodeling. They can couple electrically with cardiac myocytes and influence myocardial activation patterns. Thus, Cx43 remodeling and the level of intercellular communication in fibroblasts expressed in the infarcted heart were the subject of the present investigation.

methodsFibroblasts were isolated from both infarct scar and remote, noninfarcted regions of murine hearts 6 d after coronary ligation. Expression levels of Cx43, α-smooth muscle actin and N-cadherin were quantified by immunoblotting. Gap junctional intercellular communication was quantified by Lucifer yellow dye transfer. RESULTS AND

conclusionsFibroblasts isolated from infarcted hearts exhibited marked up-regulation of Cx43 protein expression and enhanced intercellular coupling. Exogenous administration of transforming growth factor-β (TGF-β) to fibroblast cultures from normal, non-operated hearts produced comparable up-regulation of Cx43, suggesting that increased intercellular communication between fibroblasts in infarct and peri-infarct regions may be secondary to activation of a TGF-β pathway. Unlike cardiac myocytes that down-regulate Cx43, presumably to limit intercellular transmission of biochemical mediators of ischemic injury, fibroblasts may up-regulate Cx43 to maintain electrical and metabolic coupling at a time when intercellular communication is compromised.

Indexed as

Cell CommunicationVentricular RemodelingActinsAnimalsCadherinsCells, CulturedConnexin 43ConnexinsDisease Models, AnimalFemaleFibroblastsGap JunctionsMaleMiceMice, Inbred C57BLMyocardial InfarctionActinsCadherinsCdh2 protein, mouseConnexin 43connexin 45ConnexinsGJA1 protein, mouseTransforming Growth Factor beta1

Identifiers

PMID20093048
PMCPMC2891425
OpenAlexW2008450308

What OpenQuestion holds

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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.