ArticleJACC. Basic to translational science2026
Interleukin-1β Drives Disease Progression in Arrhythmogenic Cardiomyopathy.
Article in JACC. Basic to translational science, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 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
6 citing papers in PubMed.
- Nanoparticle-Based Targeted Drug-Delivery Systems for Cardiomyopathy: Mechanisms and Therapeutic Advances.Molecules (Basel, Switzerland) · 2026Review
- Prioritizing Discovery and Advancements in Arrhythmia Therapies: NIH/NHLBI Workshop.JACC. Clinical electrophysiology · 2026Review
- Myocardial Inflammation and Arrhythmogenic Cardiomyopathy: Toward a Promising Disease-Modifying Therapy?JACC. Basic to translational science · 2026Article
- Cardiac fibroblasts in myocardial injury and heart failure.European heart journal · 2026Review
- Cardiomyocyte-Specific Plakophilin-2 Loss Is Sufficient to Induce Aging and Senescence of Nonmyocytes: Relevance to Arrhythmogenic Cardiomyopathy.Journal of the American Heart Association · 2026Article
- Cellular and Transcriptional Landscape of Human Hypoplastic Left Heart Syndrome.Research square · 2025Article
Corrections and comments
- Update of
Authors and funding
17 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Arrhythmogenic cardiomyopathy (ACM) is a genetic form of heart failure that affects 1 in 5,000 people globally and is caused by mutations in cardiac desmosomal genes including PKP2, DSP, and DSG2. Individuals with ACM suffer from ventricular arrhythmias, sudden cardiac death, and heart failure. There are few effective treatments and heart transplantation remains the best option for many affected individuals. Here we performed single nucleus RNA sequencing and spatial transcriptomics on myocardial samples from patients with ACM and control donors. We identified disease-associated spatial niches characterized by coexistence of fibrotic and inflammatory cell types and failing cardiac myocytes. The inflammatory-fibrotic niche colocalized to areas of cardiac myocyte loss and comprised FAP (fibroblast activation protein) and POSTN (periostin) expressing fibroblasts, macrophages that expressed NLRP3, and nuclear factor κB activated genes. Using homozygous Dsg2 mutant (Dsg2
Indexed as
Identifiers
What OpenQuestion 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 OpenQuestion graph.