ArticleEMBO molecular medicine2026
Sarcomeric remodelling in human heart failure unraveled by single molecule long read sequencing.
Article in EMBO molecular medicine, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
What it found
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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
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Who cites it
4 citing papers in PubMed.
- RNA splicing and cardiovascular disease: a guide for cardiologists.European heart journal · 2026Review
- Transcriptome Reprogramming in Heart Failure: The Hidden Splicing Code.Current cardiology reports · 2026Review
- Shared splicing dysregulation in heart failure associated with dilated and ischaemic cardiomyopathy and spatial specificity across cardiac regions.Cardiovascular research · 2026Article
- Leveraging Single-Cell Technologies to Advance Understanding of Myocardial Disease.Circulation research · 2026Review
Corrections and comments
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Authors and funding
18 authors.
Funding
Abstract
Dysregulation of alternative splicing - mediated by factors such as RBM20 or SLM2 - can affect proper gene isoform control, disrupting gene isoform homeostasis and underpins severe cardiomyopathy in both animal models and patients. Although innovative therapies target various sarcomeric components, the impact of isoform switching in cardiac disease remains poorly understood. Here, we applied nanopore long-read sequencing to map the full-length transcriptome of left ventricular tissue from thirteen nonfailing controls, ten patients with dilated cardiomyopathy (DCM), and ten with ischemic cardiomyopathy (ICM). Our analysis identified 78,520 transcripts, 31% of which represent novel isoforms of known genes. Notably, the transcriptomes of DCM and ICM were largely indistinguishable, indicating that end-stage heart failure is characterized by a convergent isoform landscape, irrespective of disease etiology. Among 11 prototypical sarcomere genes, 10 displayed highly significant isoform shifts (p = 5.23 × 10
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Registered trials
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