ReviewFrontiers in cardiovascular medicine2025
Research progress of connexin 43 in cardiovascular diseases.
Review in Frontiers in cardiovascular medicine, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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.
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.
Who cites it
9 citing papers in PubMed.
- Dnmt1 associatedEpigenetics · 2026Article
- Emerging Roles of Dystroglycan in Cardiac Remodeling, Fibrosis, and Heart Failure.International journal of molecular sciences · 2026Review
- From Ischemic Injury to Arrhythmogenic Substrate: Molecular and Histopathological Insights into Post-Infarction Sudden Cardiac Death.Life (Basel, Switzerland) · 2026Review
- Review
- Role of suberoylanilide hydroxamic acid and dapagliflozin on Cx43 gene expression in diabetic cardiomyopathy rat's model.Scientific reports · 2026Article
- Pro- and Anti-Inflammatory Cytokines' Implication in Right Heart Disease, Arrhythmogenesis, and Atrial Fibrillation.Biomolecules · 2026Review
- The role of autophagy in microwave radiation induced toxicity in iPSC-derived cardiomyocytes.Current research in toxicology · 2026Article
- Milk-derived extracellular vesicles in cardiovascular therapy: emerging biological functions and therapeutic perspectives.Frontiers in bioengineering and biotechnology · 2026Review
- Mitochondrial Collapse Responsible for Chagasic and Post-Ischemic Heart Failure Is Reversed by Cell Therapy Under Different Transcriptomic Topologies.Current issues in molecular biology · 2025Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Gap junctions (GJs) are critical structures for cardiac electrical signal conduction and synchronized contraction. Their fundamental components are transmembrane proteins from the connexin (Cx) family, which assemble into hexameric channels to form intercellular ion-permeable pathways, ensuring efficient electrical transmission and coordinated contraction between cardiac cells. Connexin 43 (Cx43), the most abundant connexin in the heart, serves as the primary constituent of ventricular gap junctions. Alterations in the structure, expression, distribution, and phosphorylation levels of Cx43 are closely associated with various cardiac pathologies, including arrhythmias, myocardial infarction, heart failure, ischemic cardiomyopathy, and diabetic cardiomyopathy. Thus, in-depth investigations into the biological characteristics of Cx43 are essential for elucidating the mechanisms underlying these diseases and developing potential therapeutic strategies. This review summarizes the role of Cx43 in cardiac diseases, explores its functional changes under electrophysiological and pathological conditions, and evaluates its impact on disease progression, providing theoretical insights for mechanistic studies and clinical interventions in cardiovascular diseases.
Indexed as
Identifiers
What Socratic holds
Registered trials
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.