ReviewJournal of biomedicine & biotechnology2010
Sarcomere control mechanisms and the dynamics of the cardiac cycle.
Review in Journal of biomedicine & biotechnology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 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
27 citing papers in PubMed.
- Dissecting cardiovascular disease-associated noncoding genetic variants using human iPSC models.Stem cell reports · 2025Review
- Mechanistic implications of altered protein expression in rheumatic heart disease.Heart failure reviews · 2022Review
- Organisational alteration of cardiac myofilament proteins by hyperglycaemia in mouse embryonic stem cell-derived cardiomyocytes.Journal of muscle research and cell motility · 2021Article
- Hypertrophic Cardiomyopathy: Genetic Testing and Risk Stratification.Current cardiology reports · 2021Review
- Hypertrophic Cardiomyopathy: An Overview of Genetics and Management.Biomolecules · 2019Review
- Coronary arterial vasculature in the pathophysiology of hypertrophic cardiomyopathy.Pflugers Archiv : European journal of physiology · 2019Review
- Physiological and unappreciated roles of CaMKII in the heart.Basic research in cardiology · 2018Review
- Article
- Role of myosin light chain phosphatase in cardiac physiology and pathophysiology.Journal of molecular and cellular cardiology · 2016Review
- 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
- Cardiac Troponin and Tropomyosin: Structural and Cellular Perspectives to Unveil the Hypertrophic Cardiomyopathy Phenotype.Frontiers in physiology · 2016Review
- Removal of Abnormal Myofilament O-GlcNAcylation Restores Ca2+ Sensitivity in Diabetic Cardiac Muscle.Diabetes · 2015Article
- Constitutive phosphorylation of cardiac myosin regulatory light chain in vivo.The Journal of biological chemistry · 2015Article
- The functional diversity of essential genes required for mammalian cardiac development.Genesis (New York, N.Y. : 2000) · 2014Review
- Maladaptive modifications in myofilament proteins and triggers in the progression to heart failure and sudden death.Pflugers Archiv : European journal of physiology · 2014Review
- Genetics of hypertrophic cardiomyopathy: advances and pitfalls in molecular diagnosis and therapy.The application of clinical genetics · 2014Review
- Gene regulation, alternative splicing, and posttranslational modification of troponin subunits in cardiac development and adaptation: a focused review.Frontiers in physiology · 2014Review
- Structural basis for the in situ Ca(2+) sensitization of cardiac troponin C by positive feedback from force-generating myosin cross-bridges.Archives of biochemistry and biophysics · 2013Article
- Inherited cardiomyopathies caused by troponin mutations.Journal of geriatric cardiology : JGC · 2013Article
- Integration of troponin I phosphorylation with cardiac regulatory networks.Circulation research · 2013Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
1 author.
Funding
Abstract
This review focuses on recent developments in the molecular mechanisms by which Ca activates cardiac sarcomeres and how these mechanisms play out in the cardiac cycle. I emphasize the role of mechanisms intrinsic to the sarcomeres as significant determinants of systolic elastance and ventricular stiffening during ejection. Data are presented supporting the idea that processes intrinsic to the thin filaments may promote cooperative activation of the sarcomeres and be an important factor in maintaining and modifying systolic elastance. Application of these ideas to translational medicine and rationale drug design forms an important rationale for detailed understanding of these processes.
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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.