ArticleFrontiers in cell and developmental biology2025
Genetic predisposition to immune dysregulation and extracellular matrix remodeling in cardiac arrhythmia reveals potential mediation by
Article in Frontiers in cell and developmental biology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 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
2 citing papers in PubMed.
- The role of macrophages in cardiac diseases: a review of the origins, functional diversity, and therapeutic potential.Frontiers in immunology · 2026Review
- Myocarditis with preserved left ventricular ejection fraction in-hospital convalescent phase: insights from CMR and myocardial strain analysis.Frontiers in cardiovascular medicine · 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
8 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Introduction: Cardiac arrhythmia frequently co-presents with structural abnormalities such as cardiomyopathy and myocardial fibrosis, creating a bidirectional relationship where electrical disturbances and structural remodeling exacerbate each other. Current genetic studies focus on ion channel variants, which explain part of the etiology. Molecular mechanisms underlying arrhythmias pathogenesis and its progression warrant further investigation. Methods: We performed whole-exome sequencing on 50 arrhythmia patients (21 females, 29 males), predominantly with early-onset disease (94% ≤ 35 years). We focused on exonic deleterious mutations that are rare in healthy populations. The identified recurrently mutated ( Results: We identified 132 Conclusion: Our exploratory analysis reveals how genetic variants may predispose arrhythmia patients to inflammatory and fibrotic processes. These findings may help guide future research into the molecular mechanisms underlying arrhythmia progression to structural heart disease and identify candidate pathways for therapeutic investigation.
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.