ReviewFrontiers in physiology2019
The Giant Protein Titin's Role in Cardiomyopathy: Genetic, Transcriptional, and Post-translational Modifications of TTN and Their Contribution to Cardiac Disease.
Review in Frontiers in physiology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 88 papers, 2 of them syntheses that pooled it.
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Who cites it
88 citing papers in PubMed, 2 syntheses or guidelines pooled it, 130 citations in OpenAlex.
- Guidelines on the Use of Therapeutic Apheresis in Clinical Practice-Evidence-Based Approach From the Writing Committee of the American Society for Apheresis: The Tenth Special Issue.Journal of clinical apheresis · 2026Guideline
- Multi-ancestry genetic architecture of heart failure subtypes.Nature communications · 2026Pooled it
- Alternative Splicing of TPM1 Mediated by SRPK3 Drives Cardiac Diastolic Dysfunction in Heart Failure With Preserved Ejection Fraction.Circulation · 2026Article
- Transcript-aware rare genetic variant association analyses of cardiopulmonary traits in participants from the All of Us Research Program.Nature communications · 2026Article
- Clinical and regional distribution of TTN variants in toe walking: A descriptive cohort study.Global medical genetics · 2026Article
- RNA-Based Therapies for Treating Monogenic Cardiomyopathies.The Canadian journal of cardiology · 2026Review
- Effect of chemotherapy on passenger mutations in metastatic colorectal cancer.Molecular oncology · 2026Article
- Identification of novel and known variants inFrontiers in cardiovascular medicine · 2026Article
- TTN variants in pediatric cardiomyopathy: a retrospective cohort study.Frontiers in genetics · 2026Article
- Titin Cardiomyopathy, Emerging Evidence: More Than A Big Heart.Current cardiology reports · 2025Review
- HDAC5 Inhibition as a Therapeutic Strategy for Titin Deficiency-Induced Cardiac Remodeling: Insights from Human iPSC Models.Medicines (Basel, Switzerland) · 2025Article
- Article
- QKI ensures splicing fidelity during cardiogenesis by engaging the U6 tri-snRNP to activate splicing at weak 5' splice sites.bioRxiv : the preprint server for biology · 2025Article
- Gender-specific insights into TTN mutation: potential biomarker for female risk in kidney renal clear cell carcinoma.Journal, genetic engineering & biotechnology · 2025Article
- Nonsense-Mediated mRNA Decay: Mechanisms and Recent Implications in Cardiovascular Diseases.Cells · 2025Review
- Altered expression and potential role of N6-methyladenosine mRNA methylation in abdominal aortic aneurysm mouse model.Scientific reports · 2025Article
- Rbm24-mediated post-transcriptional regulation of skeletal and cardiac muscle development, function and regeneration.Journal of muscle research and cell motility · 2025Review
- Connecting intermediate phenotypes to disease using multi-omics in heart failure.Pacific Symposium on Biocomputing. Pacific Symposium on Biocomputing · 2025Article
- Association of the TTN, PDK4, and RNF207 mutations with dilated cardiomyopathy in Dobermanns from the United Kingdom.PloS one · 2025Article
- The genomic bases of atrial fibrillation in an Ecuadorian patient: a case report.Frontiers in cardiovascular medicine · 2025Article
28 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 2 countries.
Funding
Abstract
Dilated cardiomyopathy (DCM) is a leading cause of heart failure, sudden cardiac death and heart transplant. DCM is inherited in approximately 50% of cases, in which the most frequent genetic defects are truncation variants of the titin gene ( HIGHLIGHTS: - Titin (TTN) truncation variants are the most frequent cause of dilated cardiomyopathy, one of the main causes of heart failure and heart transplant. Titin is a giant protein, and the mechanisms causing the disease are both complex and still incompletely understood.- This review discusses the role of titin in myocardial function and in disease. In particular, we discuss TTN gene structure, the complexity of genotype-phenotype correlation in human disease, the physiology of TTN and the role of post-translation modification.- Additional studies will be required to clarify whether missense variants are associated with cardiac disease. While initial studies suggested a role of non-synonymous variants in arrhythmogenic cardiomyopathy, confirmatory investigations have been hampered by the complexity of the protein structure and function.
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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.