ReviewGene2015
Cardiac myosin-binding protein C (MYBPC3) in cardiac pathophysiology.
Review in Gene, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 137 papers, 1 of them a synthesis that pooled it.
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
137 citing papers in PubMed, 1 synthesis or guideline pooled it, 225 citations in OpenAlex.
- Genome-wide analysis identifies susceptibility loci for heart failure and nonischemic cardiomyopathy subtype in the East Asian populations.PLoS genetics · 2025Pooled it
- Genetic vulnerability and dynamic mechanical stress synergistically drive sarcomere failure in human iPSC-derived cardiomyocytes.Materials today. Bio · 2026Article
- An RYR2-interacting fragment of MYBPC3 mitigates arrhythmia in human iPSC-CM and mouse models of CPVT.Molecular therapy : the journal of the American Society of Gene Therapy · 2026Article
- Oxygen-generating Microparticles Enhance Viability and Functionality of Human Pluripotent Stem Cell-derived Cardiomyocytes for Myocardial Infarction Therapy.Stem cell reviews and reports · 2026Article
- Article
- Comprehensive Pathologic and Genetic Investigation of Four Young Adults with a Short QT Interval and Sudden Unexpected Death.The Journal of molecular diagnostics : JMD · 2026Article
- STELLA: a spatial transcriptomics framework for microenvironment decoding using dynamic graph neural networks.Science China. Life sciences · 2026Article
- Is There a Unified Etiology of Hypoplastic Left Heart Syndrome? Evaluating Genetic, Structural, and Hemodynamic Models of Disease Initiation.Pathophysiology : the official journal of the International Society for Pathophysiology · 2026Review
- Variable cMyBP-C expression from cell to cell in a MYBPC3Stem cell research & therapy · 2026Article
- EchoVisuALL: From Echocardiography to Gene Discovery.bioRxiv : the preprint server for biology · 2026Article
- MYBPC3 (c.194 C > T) mutation-mediated RyR2 dysfunction contributes to pathogenic phenotypes of DCM revealed by HiPSC modeling.Cellular and molecular life sciences : CMLS · 2026Article
- Cardiac myosin-binding protein C: potential early biomarker of myocardial injury in coronary artery bypass surgery.Journal of cardiothoracic surgery · 2026Article
- Hypertrophic Cardiomyopathy is a Disease of Sarcomere Proteins.Methodist DeBakey cardiovascular journal · 2026Review
- ROS accelerates the progression of hypertrophic cardiomyopathy.Genes & diseases · 2026Article
- Generation of Clonal Cultures of Adherent or Suspension Cells Using Flat Sessile Drops for Assurance of Monoclonality.Biotechnology and bioengineering · 2025Article
- The Diagnostic Significance of Circulating Eicosanoid in Patients with Hypertrophic Cardiomyopathy.Journal of cardiovascular translational research · 2025Article
- Myosin-binding protein C slows cardiac myofibril relaxation kinetics.The Journal of physiology · 2025Article
- Current and emerging medical and surgical therapy in hypertrophic cardiomyopathy.Journal of cardiovascular imaging · 2025Review
- Spatially resolving how cMyBP-C phosphorylation and haploinsufficiency in porcine and human myofibrils affect β-cardiac myosin activity.The Journal of general physiology · 2025Article
- Pyruvate Dehydrogenase Kinase 4 Underlies the Metabolic Disorder of Cardiomyocytes in Patients With Hypertrophic Cardiomyopathy From Hypertrophy to Heart Failure.Journal of the American Heart Association · 2025Article
77 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 3 institutions in 1 country.
Funding
Abstract
More than 350 individual MYPBC3 mutations have been identified in patients with inherited hypertrophic cardiomyopathy (HCM), thus representing 40–50% of all HCM mutations, making it the most frequently mutated gene in HCM. HCM is considered a disease of the sarcomere and is characterized by left ventricular hypertrophy, myocyte disarray and diastolic dysfunction. MYBPC3 encodes for the thick filament associated protein cardiac myosin-binding protein C (cMyBP-C), a signaling node in cardiac myocytes that contributes to the maintenance of sarcomeric structure and regulation of contraction and relaxation. This review aims to provide a succinct overview of how mutations in MYBPC3 are considered to affect the physiological function of cMyBP-C, thus causing the deleterious consequences observed inHCM patients. Importantly, recent advances to causally treat HCM by repairing MYBPC3 mutations by gene therapy are discussed here, providing a promising alternative to heart transplantation for patients with a fatal form of neonatal cardiomyopathy due to bi-allelic truncating MYBPC3 mutations.
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.