ReviewPflugers Archiv : European journal of physiology2011
Diastolic myofilament dysfunction in the failing human heart.
Review in Pflugers Archiv : European journal of physiology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 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
28 citing papers in PubMed.
- Depressed myocardial cross-bridge cycling kinetics in a female guinea pig model of diastolic heart failure.The Journal of general physiology · 2023Article
- Article
- Sarcomeres Morphology and Z-Line Arrangement Disarray Induced by Ventricular Premature Contractions through the Rac2/Cofilin Pathway.International journal of molecular sciences · 2021Article
- Need for Speed: The Importance of Physiological Strain Rates in Determining Myocardial Stiffness.Frontiers in physiology · 2021Article
- Anesthetic Agents Isoflurane and Propofol Decrease Maximal CaThe Journal of pharmacology and experimental therapeutics · 2019Article
- As time flies by: Investigating cardiac aging in the short-lived Drosophila model.Biochimica et biophysica acta. Molecular basis of disease · 2019Review
- Monophosphorylation of cardiac troponin-I at Ser-23/24 is sufficient to regulate cardiac myofibrillar CaThe Journal of biological chemistry · 2018Article
- The continuing evolution of cardiac troponin I biomarker analysis: from protein to proteoform.Expert review of proteomics · 2017Review
- Z-disc protein CHAPb induces cardiomyopathy and contractile dysfunction in the postnatal heart.PloS one · 2017Article
- TSH inhibits SERCA2a and the PKA/PLN pathway in rat cardiomyocytes.Oncotarget · 2016Article
- The contributions of cardiac myosin binding protein C and troponin I phosphorylation to β-adrenergic enhancement of in vivo cardiac function.The Journal of physiology · 2016Article
- Article
- Cell- and molecular-level mechanisms contributing to diastolic dysfunction in HFpEF.Journal of applied physiology (Bethesda, Md. : 1985) · 2015Review
- Pathomechanisms in heart failure: the contractile connection.Journal of muscle research and cell motility · 2015Review
- The cardiac-specific N-terminal region of troponin I positions the regulatory domain of troponin C.Proceedings of the National Academy of Sciences of the United States of America · 2014Article
- Troponin I phosphorylation in human myocardium in health and disease.Netherlands heart journal : monthly journal of the Netherlands Society of Cardiology and the Netherlands Heart Foundation · 2014Article
- Contractile properties of the right atrial myofilaments in patients with myxomatous mitral valve degeneration.BMC cardiovascular disorders · 2014Article
- Phosphorylation of protein kinase C sites Ser42/44 decreases Ca(2+)-sensitivity and blunts enhanced length-dependent activation in response to protein kinase A in human cardiomyocytes.Archives of biochemistry and biophysics · 2014Article
- Protein changes contributing to right ventricular cardiomyocyte diastolic dysfunction in pulmonary arterial hypertension.Journal of the American Heart Association · 2014Article
- Maladaptive modifications in myofilament proteins and triggers in the progression to heart failure and sudden death.Pflugers Archiv : European journal of physiology · 2014Review
Corrections and comments
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Authors and funding
1 author.
Funding
No grant is acknowledged in the PubMed record.
Abstract
In recent years, it has become evident that heart failure is not solely due to reduced contractile performance of the heart muscle as impaired relaxation is evident in almost all heart failure patients. In more than half of all heart failure patients, diastolic dysfunction is the major cardiac deficit. These heart failure patients have normal (or preserved) left ventricular ejection fraction, but impaired diastolic function evident from increased left ventricular end-diastolic pressure. Perturbations at the cellular level which cause impaired relaxation of the heart muscle involve changes in Ca(2+)-handling proteins, extracellular matrix components, and myofilament properties. The present review discusses the deficits in myofilament function observed in human heart failure and the most likely underlying causal protein changes. Moreover, the consequences of impaired myofilament function for in vivo diastolic dysfunction are discussed taking into account the reported changes in Ca(2+) handling.
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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.