ArticleCirculation. Cardiovascular imaging2012
Cardiac myosin binding protein C insufficiency leads to early onset of mechanical dysfunction.
Article in Circulation. Cardiovascular imaging, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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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.
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Who cites it
17 citing papers in PubMed, 23 citations in OpenAlex.
- Myosin motor dynamics and cardiac function: Insights from in vivo small-angle X-ray scattering and pressure-volume analysis.The Journal of physiology · 2026Article
- Cardiac MRI Strain as an Early Indicator of Myocardial Dysfunction in Hypertrophic Cardiomyopathy.International journal of molecular sciences · 2025Article
- MYBPC3-c.772G>A mutation results in haploinsufficiency and altered myosin cycling kinetics in a patient induced stem cell derived cardiomyocyte model of hypertrophic cardiomyopathy.Journal of molecular and cellular cardiology · 2024Article
- Insights into the Novel Cardiac Biomarker in Acute Heart Failure: Mybp-C.Life (Basel, Switzerland) · 2024Article
- Strategies for targeting the cardiac sarcomere: avenues for novel drug discovery.Expert opinion on drug discovery · 2020Review
- Cardiac Myosin Binding Protein-C Phosphorylation Modulates Myofilament Length-Dependent Activation.Frontiers in physiology · 2016Article
- Molecular effects of the myosin activator omecamtiv mecarbil on contractile properties of skinned myocardium lacking cardiac myosin binding protein-C.Journal of molecular and cellular cardiology · 2015Article
- Quantification of regional myocardial wall motion by cardiovascular magnetic resonance.Quantitative imaging in medicine and surgery · 2014Review
- The contribution of cardiac myosin binding protein-c Ser282 phosphorylation to the rate of force generation and in vivo cardiac contractility.The Journal of physiology · 2014Article
- Phosphorylation of cMyBP-C affects contractile mechanisms in a site-specific manner.Biophysical journal · 2014Article
- Contractile dysfunction in a mouse model expressing a heterozygous MYBPC3 mutation associated with hypertrophic cardiomyopathy.American journal of physiology. Heart and circulatory physiology · 2014Article
- Cardiac myosin binding protein-C: a novel sarcomeric target for gene therapy.Pflugers Archiv : European journal of physiology · 2014Article
- Length-dependent changes in contractile dynamics are blunted due to cardiac myosin binding protein-C ablation.Frontiers in physiology · 2014Article
- Cardiac myosin binding protein C phosphorylation affects cross-bridge cycle's elementary steps in a site-specific manner.PloS one · 2014Article
- Functional dissection of myosin binding protein C phosphorylation.Journal of molecular and cellular cardiology · 2013Article
- Impaired contractile function due to decreased cardiac myosin binding protein C content in the sarcomere.American journal of physiology. Heart and circulatory physiology · 2013Article
- In vivo cardiac myosin binding protein C gene transfer rescues myofilament contractile dysfunction in cardiac myosin binding protein C null mice.Circulation. Heart failure · 2012Article
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
backgroundDecreased expression of cardiac myosin binding protein C (cMyBPC) as a result of genetic mutations may contribute to the development of hypertrophic cardiomyopathy (HCM); however, the mechanisms that link cMyBPC expression and HCM development, especially contractile dysfunction, remain unclear. METHODS AND
resultsWe evaluated cardiac mechanical function in vitro and in vivo in young mice (8-10 weeks of age) carrying no functional cMyBPC alleles (cMyBPC(-/-)) or 1 functional cMyBPC allele (cMyBPC(±)). Skinned myocardium isolated from cMyBPC(-/-) hearts displayed significant accelerations in stretch activation cross-bridge kinetics. Cardiac MRI studies revealed severely depressed in vivo left ventricular (LV) magnitude and rates of LV wall strain and torsion compared with wild-type (WT) mice. Heterozygous cMyBPC(±) hearts expressed 23±5% less cMyBPC than WT hearts but did not display overt hypertrophy. Skinned myocardium isolated from cMyBPC(±) hearts displayed small accelerations in the rate of stretch induced cross-bridge recruitment. MRI measurements revealed reductions in LV torsion and circumferential strain, as well reduced circumferential strain rates in early systole and diastole.
conclusionsModest decreases in cMyBPC expression in the mouse heart result in early-onset subtle changes in cross-bridge kinetics and in vivo LV mechanical function, which could contribute to the development of HCM later in life.
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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.