ArticleNetherlands heart journal : monthly journal of the Netherlands Society of Cardiology and the Netherlands Heart Foundation2014
Troponin I phosphorylation in human myocardium in health and disease.
Article in Netherlands heart journal : monthly journal of the Netherlands Society of Cardiology and the Netherlands Heart Foundation, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 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.
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Who cites it
22 citing papers in PubMed, 36 citations in OpenAlex.
- Troponin: biology, molecular mechanisms, and multidimensional clinical applications.Molecular biomedicine · 2026Review
- An ALPK3 truncation variant causing autosomal dominant hypertrophic cardiomyopathy is partially rescued by mavacamten.Scientific reports · 2025Article
- Rethinking of phosphodiesterase 5 inhibition: the old, the new and the perspective in human health.Frontiers in endocrinology · 2024Review
- Dysregulated Autophagy and Sarcomere Dysfunction in Patients With Heart Failure With Co-Occurrence of P63A and P380SJournal of the American Heart Association · 2023Article
- Cardiac muscle physiology.BJA education · 2023Review
- Thin filament regulation of cardiac muscle power output: Implications for targets to improve human failing hearts.The Journal of general physiology · 2023Article
- Article
- Titin-truncating mutations associated with dilated cardiomyopathy alter length-dependent activation and its modulation via phosphorylation.Cardiovascular research · 2022Article
- Cyclic GMP and PKG Signaling in Heart Failure.Frontiers in pharmacology · 2022Review
- Article
- Cardiomyocyte contractile impairment in heart failure results from reduced BAG3-mediated sarcomeric protein turnover.Nature communications · 2021Article
- Robustness and Ruggedness of Isoelectric Focusing and Superficially Porous Liquid Chromatography with Fourier Transform Mass Spectrometry.Journal of the American Society for Mass Spectrometry · 2021Article
- Regulation of Myofilament Contractile Function in Human Donor and Failing Hearts.Frontiers in physiology · 2020Article
- Defining decreased protein succinylation of failing human cardiac myofibrils in ischemic cardiomyopathy.Journal of molecular and cellular cardiology · 2020Article
- Constructing a structural model of troponin using site-directed spin labeling: EPR and PRE-NMR.Biophysical reviews · 2019Review
- Functional cardiac orexin receptors: role of orexin-B/orexin 2 receptor in myocardial protection.Clinical science (London, England : 1979) · 2018Article
- Cardiomyopathies and Related Changes in Contractility of Human Heart Muscle.International journal of molecular sciences · 2018Review
- The continuing evolution of cardiac troponin I biomarker analysis: from protein to proteoform.Expert review of proteomics · 2017Review
- Cross-Talk Between Insulin Signaling and G Protein-Coupled Receptors.Journal of cardiovascular pharmacology · 2017Review
- Influence of apelin-12 on troponin levels and the rate of MACE in STEMI patients.BMC cardiovascular disorders · 2017Observational
Corrections and comments
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Authors and funding
4 authors at 4 institutions in 2 countries.
Funding
Abstract
Cardiac troponin I (cTnI) is well known as a biomarker for the diagnosis of myocardial damage. However, because of its central role in the regulation of contraction and relaxation in heart muscle, cTnI may also be a potential target for the treatment of heart failure. Studies in rodent models of cardiac disease and human heart samples showed altered phosphorylation at various sites on cTnI (i.e. site-specific phosphorylation). This is caused by altered expression and/or activity of kinases and phosphatases during heart failure development. It is not known whether these (transient) alterations in cTnI phosphorylation are beneficial or detrimental. Knowledge of the effects of site-specific cTnI phosphorylation on cardiomyocyte contractility is therefore of utmost importance for the development of new therapeutic strategies in patients with heart failure. In this review we focus on the role of cTnI phosphorylation in the healthy heart upon activation of the beta-adrenergic receptor pathway (as occurs during increased stress and exercise) and as a modulator of the Frank-Starling mechanism. Moreover, we provide an overview of recent studies which aimed to reveal the functional consequences of changes in cTnI phosphorylation in cardiac disease.
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.