Evidence map›Paper›PMID 26073311›Full record

ReviewPharmacology & therapeutics2015

Connexin 43 is an emerging therapeutic target in ischemia/reperfusion injury, cardioprotection and neuroprotection.

Rainer Schulz, Philipp Maximilian Görge, Anikó Görbe, Péter Ferdinandy, Paul D Lampe, Luc Leybaert

Open access · greenAbstract readReview
In one paragraph

Review in Pharmacology & therapeutics, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 134 papers.

0numbers the graph read from it
0cells of the map it votes in
134citing papers in PubMed
11.6field-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

134 citing papers in PubMed, 226 citations in OpenAlex.

  1. Review
  2. COeLife · 2026
    Article
  3. Review
  4. Article
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  6. 2-Aminoethoxydiphenyl borate induces arrhythmias via Cx43-S282 dephosphorylation.In vitro cellular & developmental biology. Animal · 2026
    Article
  7. Review
  8. Article
  9. Modulation of Redox-Sensitive Cardiac Ion Channels.Antioxidants (Basel, Switzerland) · 2025
    Review
  10. Review
  11. Review
  12. Article
  13. Article
  14. Review
  15. Review
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  19. Article
  20. Article

74 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

6 authors at 5 institutions in 4 countries.

Rainer SchulzInstitut für Physiologie, JustusLiebig Universität Giessen, Gießen, Germany. Electronic address: rainer.schulz@physiologie.med.uni-giessen.de.
Philipp Maximilian GörgeInstitut für Physiologie, JustusLiebig Universität Giessen, Gießen, Germany.
Anikó GörbeCardiovascular Research Group, Department of Biochemistry, Faculty of Medicine, University of Szeged, Hungary; Pharmahungary Group, Szeged, Hungary.
Péter FerdinandyDepartment of Pharmacology and Pharmacotherapy, Semmelweis University, Budapest, Hungary; Pharmahungary Group, Szeged, Hungary.
Paul D LampeFred Hutchinson Cancer Research Center, Seattle, WA, USA.
Luc LeybaertPhysiology Group, Department Basic Medical Sciences, Ghent University, Belgium.
University of Giessen · DEFred Hutch Cancer Center · USGhent University · BESemmelweis University · HUUniversity of Szeged · HU

Funding

PHOSPHORYLATION OF GAP JUNCTION PROTEINSR01GM055632 · NIGMS · FRED HUTCHINSON CANCER RESEARCH CENTER · PI LAMPE, PAUL D. · 1997 to 2017
$6.1M
NIGMS NIH HHS GM55632NIGMS NIH HHS R01 GM055632
6 · The paper itself

Abstract

Connexins are widely distributed proteins in the body that are crucially important for heart and brain functions. Six connexin subunits form a connexon or hemichannel in the plasma membrane. Interactions between two hemichannels in a head-to-head arrangement result in the formation of a gap junction channel. Gap junctions are necessary to coordinate cell function by passing electrical current flow between heart and nerve cells or by allowing exchange of chemical signals and energy substrates. Apart from its localization at the sarcolemma of cardiomyocytes and brain cells, connexins are also found in the mitochondria where they are involved in the regulation of mitochondrial matrix ion fluxes and respiration. Connexin expression is affected by age and gender as well as several pathophysiological alterations such as hypertension, hypertrophy, diabetes, hypercholesterolemia, ischemia, post-myocardial infarction remodeling or heart failure, and post-translationally connexins are modified by phosphorylation/de-phosphorylation and nitros(yl)ation which can modulate channel activity. Using knockout/knockin technology as well as pharmacological approaches, one of the connexins, namely connexin 43, has been identified to be important for cardiac and brain ischemia/reperfusion injuries as well as protection from it. Therefore, the current review will focus on the importance of connexin 43 for irreversible injury of heart and brain tissues following ischemia/reperfusion and will highlight the importance of connexin 43 as an emerging therapeutic target in cardio- and neuroprotection.

Indexed as

AnimalsBrainCardiotonic AgentsConnexin 43HeartHumansModels, MolecularMolecular Targeted TherapyMyocardiumNeuroprotectionReperfusion InjurySpinal Cord InjuriesCardiotonic AgentsConnexin 43BrainCardioprotectionConnexin 43HeartMitochondriaNeuroprotection

Identifiers

PMID26073311
PMCPMC4599355
OpenAlexW642235081

What Socratic 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 Socratic graph.