ReviewPflugers Archiv : European journal of physiology2014
Cardiac myosin-binding protein-C is a critical mediator of diastolic function.
Review in Pflugers Archiv : European journal of physiology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 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
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
21 citing papers in PubMed, 39 citations in OpenAlex.
- Influence of Clinical Aspects and Genetic Factors on Feline HCM Severity and Development.Veterinary sciences · 2024Article
- Reference values and biological determinants for cardiac myosin-binding protein C concentrations assessed with an enzyme-linked immunosorbent assay.Journal of medical biochemistry · 2023Article
- Synthetic growth hormone-releasing hormone agonist ameliorates the myocardial pathophysiology characteristic of heart failure with preserved ejection fraction.Cardiovascular research · 2023Article
- Cardiovascular disease risk prediction in scleroderma.Revista da Associacao Medica Brasileira (1992) · 2023Article
- Lipids: a Potential Molecular Pathway Towards Diastolic Dysfunction in Youth-Onset Type 2 Diabetes.Current atherosclerosis reports · 2022Review
- Inhibiting cardiac myeloperoxidase alleviates the relaxation defect in hypertrophic cardiomyocytes.Cardiovascular research · 2022Article
- Interventricular Differences of Signaling Pathways-Mediated Regulation of Cardiomyocyte Function in Response to High Oxidative Stress in the Post-Ischemic Failing Rat Heart.Antioxidants (Basel, Switzerland) · 2021Article
- Making waves: A proposed new role for myosin-binding protein C in regulating oscillatory contractions in vertebrate striated muscle.The Journal of general physiology · 2021Article
- Left ventricular dysfunction in heart failure with preserved ejection fraction-molecular mechanisms and impact on right ventricular function.Cardiovascular diagnosis and therapy · 2020Review
- Late-life restoration of mitochondrial function reverses cardiac dysfunction in old mice.eLife · 2020Article
- A Novel "Cut and Paste" Method for In Situ Replacement of cMyBP-C Reveals a New Role for cMyBP-C in the Regulation of Contractile Oscillations.Circulation research · 2020Article
- Sphingosine-1-Phosphate Receptor Modulator, FTY720, Improves Diastolic Dysfunction and Partially Reverses Atrial Remodeling in a Tm-E180G Mouse Model Linked to Hypertrophic Cardiomyopathy.Circulation. Heart failure · 2019Article
- Point mutations in the tri-helix bundle of the M-domain of cardiac myosin binding protein-C influence systolic duration and delay cardiac relaxation.Journal of molecular and cellular cardiology · 2018Article
- Myocardial transcription factors in diastolic dysfunction: clues for model systems and disease.Heart failure reviews · 2016Review
- Site-directed spectroscopy of cardiac myosin-binding protein C reveals effects of phosphorylation on protein structural dynamics.Proceedings of the National Academy of Sciences of the United States of America · 2016Article
- The genetic basis of hypertrophic cardiomyopathy in cats and humans.Journal of veterinary cardiology : the official journal of the European Society of Veterinary Cardiology · 2015Review
- Cardiac-specific deletion of protein phosphatase 1β promotes increased myofilament protein phosphorylation and contractile alterations.Journal of molecular and cellular cardiology · 2015Article
- A mouse model of heart failure with preserved ejection fraction due to chronic infusion of a low subpressor dose of angiotensin II.American journal of physiology. Heart and circulatory physiology · 2015Article
- Chronic Rho-kinase inhibition improves left ventricular contractile dysfunction in early type-1 diabetes by increasing myosin cross-bridge extension.Cardiovascular diabetology · 2015Article
- Phosphorylation of cardiac Myosin-binding protein-C is a critical mediator of diastolic function.Circulation. Heart failure · 2015Article
Corrections and comments
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Authors and funding
5 authors at 3 institutions in 1 country.
Funding
Abstract
Diastolic dysfunction prominently contributes to heart failure with preserved ejection fraction (HFpEF). Owing partly to inadequate understanding, HFpEF does not have any effective treatments. Cardiac myosin-binding protein-C (cMyBP-C), a component of the thick filament of heart muscle that can modulate cross-bridge attachment/detachment cycling process by its phosphorylation status, appears to be involved in the diastolic dysfunction associated with HFpEF. In patients, cMyBP-C mutations are associated with diastolic dysfunction even in the absence of hypertrophy. cMyBP-C deletion mouse models recapitulate diastolic dysfunction despite in vitro evidence of uninhibited cross-bridge cycling. Reduced phosphorylation of cMyBP-C is also associated with diastolic dysfunction in patients. Mouse models of reduced cMyBP-C phosphorylation exhibit diastolic dysfunction while cMyBP-C phosphorylation mimetic mouse models show enhanced diastolic function. Thus, cMyBP-C phosphorylation mediates diastolic function. Experimental results of both cMyBP-C deletion and reduced cMyBP-C phosphorylation causing diastolic dysfunction suggest that cMyBP-C phosphorylation level modulates cross-bridge detachment rate in relation to ongoing attachment rate to mediate relaxation. Consequently, alteration in cMyBP-C regulation of cross-bridge detachment is a key mechanism that causes diastolic dysfunction. Regardless of the exact molecular mechanism, ample clinical and experimental data show that cMyBP-C is a critical mediator of diastolic function. Furthermore, targeting cMyBP-C phosphorylation holds potential as a future treatment for 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.