Evidence map›Paper›PMID 40149906›Full record

ReviewBiomolecules2025

Overexpression of Cx43: Is It an Effective Approach for the Treatment of Cardiovascular Diseases?

Kerstin Boengler, Beatrice Mantuano, Shira Toledano, Ofer Binah, Rainer Schulz

Abstract readReview
In one paragraph

Review in Biomolecules, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed, 1 pooled it
–field-weighted citation impact
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

4 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
  2. Dnmt1 associatedEpigenetics · 2026
    Article
  3. Article
  4. Review
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

5 authors.

Kerstin BoenglerInstitute of Physiology, Justus-Liebig University, 35392 Giessen, Germany.
Beatrice MantuanoDepartment of Clinical and Biological Sciences, University of Torino, 10125 Torino, Italy.ORCID 0009-0000-3263-7944
Shira ToledanoDepartment of Physiology, Biophysics and Systems Biology, Rappaport Faculty of Medicine, Technion-Israel Institute of Technology, Haifa 3190601, Israel.ORCID 0000-0002-2590-6066
Ofer BinahDepartment of Physiology, Biophysics and Systems Biology, Rappaport Faculty of Medicine, Technion-Israel Institute of Technology, Haifa 3190601, Israel.
Rainer SchulzInstitute of Physiology, Justus-Liebig University, 35392 Giessen, Germany.ORCID 0000-0003-3017-0476

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

In the heart, Connexin 43 (Cx43) is involved in intercellular communication through gap junctions and exosomes. In addition, Cx43-formed hemichannels at the plasma membrane are important for ion homeostasis and cellular volume regulation. Through its localization within nuclei and mitochondria, Cx43 influences the function of the respective organelles. Several cardiovascular diseases such as heart failure, ischemia/reperfusion injury, hypertrophic cardiomyopathy and arrhythmias are characterized by Cx43 downregulation and a dysregulated Cx43 function. Accordingly, a putative therapeutic approach of these diseases would include the induction of Cx43 expression in the damaged heart, albeit such induction may have both beneficial and detrimental effects. In this review we discuss the consequences of increasing cardiac Cx43 expression, and discuss this manipulation as a strategy for the treatment of cardiovascular diseases.

Indexed as

Cardiovascular DiseasesConnexin 43AnimalsGap JunctionsHumansConnexin 43cardiac diseaseconnexingap junctionhemichannelmitochondria

Identifiers

PMID40149906
PMCPMC11940156

What Socratic holds

Textmetadata
LicenceCC BY
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.