ArticleJournal of molecular medicine (Berlin, Germany)2016
Reducing RBM20 activity improves diastolic dysfunction and cardiac atrophy.
Article in Journal of molecular medicine (Berlin, Germany), 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.
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Who cites it
35 citing papers in PubMed, 45 citations in OpenAlex.
- RNA splicing and cardiovascular disease: a guide for cardiologists.European heart journal · 2026Review
- RBM20 isoform regulation by independent transcription start sites adapts alternative splicing in development and disease.Nature communications · 2026Article
- Mending the Achilles heels of titin in cardiac and musculoskeletal disease.Biophysical reviews · 2026Review
- Review
- Antisense-mediated regulation of exon usage in the elastic spring region of Titin modulates sarcomere function.Cardiovascular research · 2025Article
- RNA binding proteins in cardiovascular development and disease.Current topics in developmental biology · 2024Article
- Titin: roles in cardiac function and diseases.Frontiers in physiology · 2024Review
- Cardiac splicing as a diagnostic and therapeutic target.Nature reviews. Cardiology · 2023Review
- Landscape of RNA-binding proteins in diagnostic utility, immune cell infiltration and PANoptosis features of heart failure.Frontiers in genetics · 2022Article
- RBM20, a Therapeutic Target to Alleviate Myocardial StiffnessFrontiers in cardiovascular medicine · 2022Review
- The titin N2B and N2A regions: biomechanical and metabolic signaling hubs in cross-striated muscles.Biophysical reviews · 2021Review
- Cardiac sarcomere mechanics in health and disease.Biophysical reviews · 2021Review
- New Insights in RBM20 Cardiomyopathy.Current heart failure reports · 2020Review
- Modifications of Titin Contribute to the Progression of Cardiomyopathy and Represent a Therapeutic Target for Treatment of Heart Failure.Journal of clinical medicine · 2020Review
- Structural basis of UCUU RNA motif recognition by splicing factor RBM20.Nucleic acids research · 2020Article
- Review
- mRNA Metabolism in Cardiac Development and Disease: Life After Transcription.Physiological reviews · 2020Review
- Deleting Titin's C-Terminal PEVK Exons Increases Passive Stiffness, Alters Splicing, and Induces Cross-Sectional and Longitudinal Hypertrophy in Skeletal Muscle.Frontiers in physiology · 2020Article
- Resolving titin's lifecycle and the spatial organization of protein turnover in mouse cardiomyocytes.Proceedings of the National Academy of Sciences of the United States of America · 2019Article
- End-diastolic force pre-activates cardiomyocytes and determines contractile force: role of titin and calcium.The Journal of physiology · 2019Article
Corrections and comments
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Authors and funding
5 authors at 3 institutions in 2 countries.
Funding
Abstract
Impaired diastolic filling is a main contributor to heart failure with preserved ejection fraction (HFpEF), a syndrome with increasing prevalence and no treatment. Both collagen and the giant sarcomeric protein titin determine diastolic function. Since titin's elastic properties can be adjusted physiologically, we evaluated titin-based stiffness as a therapeutic target. We adjusted RBM20-dependent cardiac isoform expression in the titin N2B knockout mouse with increased ventricular stiffness. A ~50 % reduction of RBM20 activity does not only maintain cardiac filling in diastole but also ameliorates cardiac atrophy and thus improves cardiac function in the N2B-deficient heart. Reduced RBM20 activity partially normalized gene expression related to muscle development and fatty acid metabolism. The adaptation of cardiac growth was related to hypertrophy signaling via four-and-a-half lim-domain proteins (FHLs) that translate mechanical input into hypertrophy signals. We provide a novel link between cardiac isoform expression and trophic signaling via FHLs and suggest cardiac splicing as a therapeutic target in diastolic dysfunction. KEY MESSAGE: Increasing the length of titin isoforms improves ventricular filling in heart disease. FHL proteins are regulated via RBM20 and adapt cardiac growth. RBM20 is a therapeutic target in diastolic dysfunction.
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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.