ArticleFrontiers in physiology2025
Ion channels and atrial fibrillation: mitophagy as a key mediator.
Article in Frontiers in physiology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 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
3 citing papers in PubMed.
- Integrated Genomic and Transcriptomic Analysis Reveals the Genetic Basis and Causal Association Between Obesity and Atrial Fibrillation.Diabetes, obesity & metabolism · 2026Article
- Macrophage migration inhibitory factor in atrial fibrillation.Frontiers in immunology · 2026Review
- Oxidative Stress, Mitochondrial Homeostasis, and Sirtuins in Atrial Fibrillation.International journal of molecular sciences · 2025Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
11 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background: The prevalence of atrial fibrillation (AF) is increasing due to the aging population. Mitophagy is crucial for maintaining cardiomyocyte function, while ion channels play a key role in cardiac electrical activity. Dysfunction of ion channels can trigger AF. However, the role of mitophagy-related ion channel genes in AF remains unclear. Methods: AF-related datasets GSE41177 and GSE79768 were merged and batch-corrected for differential expression analysis. Mitophagy-related and ion channel-related genes were obtained from the MsigDB and GeneCards databases. Immune infiltration and functional enrichment analyses were performed. Sixty-five machine learning models were developed to identify Hub genes, with the optimal model selected based on receiver operating characteristic curves, F1 scores, and accuracy. An acute electrical remodeling model of atrial tachyarrhythmia was established in Sprague-Dawley rats by administering a mixture of acetylcholine-calcium chloride for 7 days. Hematoxylin-eosin, Masson, and Sirius red staining were used to detect histopathologic changes in the atrial myocardium. The expression of AF-related mitophagy ion channel genes and proteins was measured by qRT-PCR and Western blotting. Results: A total of 444 differentially expressed genes in AF were identified, and 9 AF-related mitophagy ion channel genes (AFRMICGs) were obtained (BAX, CTNNB1, DPYSL2, EPHX1, GLUL, GNB2, MIF, MYC, TLR4). Functional enrichment analysis indicated that the pathogenesis of AF is related to inflammation, immune response, ion channels, apoptosis, and various organelles and is associated with the PI3K/AKT, NF-kappa B, JAK-STAT, and mTOR pathways. Immune infiltration analysis showed higher resting dendritic cells and neutrophils and lower follicular helper T cells, M2 macrophages, and activated dendritic cells in AF patients. The glmBoost + Lasso model identified 4 Hub genes: BAX, GLUL, MIF, and TLR4. Conclusion: BAX, MIF, and TLR4 are key genes linking mitophagy and ion channels in AF, which appear to influence the immune microenvironment by modulating immune cell infiltration.
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.