Evidence map›Paper›PMID 26627143›Full record

ReviewProgress in biophysics and molecular biology2016

Cardiac conduction in isolated hearts of genetically modified mice--Connexin43 and salts.

Sharon A George, Steven Poelzing

Abstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in Progress in biophysics and molecular biology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
1.8field-weighted citation impact, top 15% 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

19 citing papers in PubMed, 31 citations in OpenAlex.

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  17. Revealing the Concealed Nature of Long-QT Type 3 Syndrome.Circulation. Arrhythmia and electrophysiology · 2017
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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 1 country.

Sharon A GeorgeDepartment of Biomedical Engineering and Mechanics, Virginia Tech Carilion Research Institute, and Center for Heart and Regenerative Medicine, Virginia Polytechnic Institute and State University, Blacksburg, VA, USA. Electronic address: sharonag@vt.edu.
Steven PoelzingDepartment of Biomedical Engineering and Mechanics, Virginia Tech Carilion Research Institute, and Center for Heart and Regenerative Medicine, Virginia Polytechnic Institute and State University, Blacksburg, VA, USA. Electronic address: poelzing@vtc.vt.edu.
Virginia Tech · US

Funding

Role of the Extracellular Space as a Modulator of the Cardiac Gap Junction - Conduction Velocity RelationshipR01HL102298 · NHLBI · VIRGINIA POLYTECHNIC INST AND ST UNIV · PI POELZING, STEVEN · 2011 to 2020
$3.9M
NHLBI NIH HHS R01 HL102298NHLBI NIH HHS R01-HL102298
6 · The paper itself

Abstract

Physiologic variations in perfusate composition have been identified as a new and important modulator of cardiac conduction velocity (CV), particularly when gap junctions (GJ) are reduced. We recently demonstrated in ex vivo hearts that perfusates with low sodium and high potassium preferentially slow ventricular CV in mice genetically engineered to express 50% less of the gap junction protein, connexin43 (Cx43). We also reported the possible role of calcium in modulating CV. In this review we discuss previous murine studies that explored the CV-GJ relationship in isolated mouse heart preparations with approximately 50% reduced Cx43. Studies were grouped according to the type of perfusate utilized, and CV during GJ uncoupling was compared. Studies in Group A preferentially used perfusates with low sodium, high potassium and non-physiologic calcium, and found CV slows and arrhythmias increase in mouse hearts with reduced Cx43. Studies in Group B used solutions with high sodium, low potassium and physiologic calcium, and did not observe CV slowing nor increased arrhythmia risk with loss of Cx3. Studies in Group C used solutions with low sodium, low potassium, physiologic calcium, creatine, taurine, and insulin. CV slowing was not observed, nor was arrhythmia risk increased with loss of Cx43. We suggest that perfusate ion composition may be a major determinant of whether CV slows when Cx43 is reduced. Furthermore, the review of these studies highlights important theoretical developments in the understanding of cardiac conduction and suggests that ionic milieu can conceal electrophysiologic remodeling secondary to reduced Cx43 expression as occurs in many cardiac diseases.

Indexed as

AnimalsArrhythmias, CardiacConnexin 43Gap JunctionsHeart Conduction SystemHumansMiceMice, TransgenicSaltsConnexin 43SaltsConductionConduction reserveConnexin43Ephaptic couplingPerfusate

Identifiers

PMID26627143
PMCPMC4808347
OpenAlexW2184066959

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.