ReviewFrontiers in physiology2014
Investigating the role of uncoupling of troponin I phosphorylation from changes in myofibrillar Ca(2+)-sensitivity in the pathogenesis of cardiomyopathy.
Review in Frontiers in physiology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 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
47 citing papers in PubMed, 61 citations in OpenAlex.
- Dual role of Tropomyosin-R160 in thin filament regulation: Insights into phosphorylation-dependent cardiac relaxation and cardiomyopathy mechanisms.Archives of biochemistry and biophysics · 2025Article
- 5,7-Dimethoxychroman-3-yl 4-methoxybenzoate Has a Unique Effect upon the Modulation of Mutant Cardiac Muscle Thin Filament Function and Dynamics due to Phosphorylation of Troponin I.ACS pharmacology & translational science · 2025Article
- Three Novel Pathogenic Variants in Unrelated Vietnamese Patients with Cardiomyopathy.Diagnostics (Basel, Switzerland) · 2024Article
- Focus on cardiac troponin complex: From gene expression to cardiomyopathy.Genes & diseases · 2024Review
- Activation of IPAmerican journal of physiology. Heart and circulatory physiology · 2024Article
- Emerging Concepts of Mechanisms Controlling Cardiac Tension: Focus on Familial Dilated Cardiomyopathy (DCM) and Sarcomere-Directed Therapies.Biomedicines · 2024Review
- Nutraceuticals silybin B, resveratrol, and epigallocatechin-3 gallate-bind to cardiac muscle troponin to restore the loss of lusitropy caused by cardiomyopathy mutationsFrontiers in physiology · 2024Article
- Modulation of Structure and Dynamics of Cardiac Troponin by Phosphorylation and Mutations Revealed by Molecular Dynamics Simulations.The journal of physical chemistry. B · 2023Article
- Recent studies of the molecular mechanism of lusitropy due to phosphorylation of cardiac troponin I by protein kinase A.Journal of muscle research and cell motility · 2023Review
- Myofilament-associated proteins with intrinsic disorder (MAPIDs) and their resolution by computational modeling.Quarterly reviews of biophysics · 2023Review
- Critical Evaluation of Current Hypotheses for the Pathogenesis of Hypertrophic Cardiomyopathy.International journal of molecular sciences · 2022Review
- Suppression of lusitropy as a disease mechanism in cardiomyopathies.Frontiers in cardiovascular medicine · 2022Review
- Functional and Molecular Characterisation of Heart Failure Progression in Mice and the Role of Myosin Regulatory Light Chains in the Recovery of Cardiac Muscle Function.International journal of molecular sciences · 2021Article
- The updated view on induced pluripotent stem cells for cardiovascular precision medicine.Pflugers Archiv : European journal of physiology · 2021Review
- Resveratrol Prevents Right Ventricle Dysfunction, Calcium Mishandling, and Energetic Failure via SIRT3 Stimulation in Pulmonary Arterial Hypertension.Oxidative medicine and cellular longevity · 2021Article
- Small Molecules acting on Myofilaments as Treatments for Heart and Skeletal Muscle Diseases.International journal of molecular sciences · 2020Review
- Troponin structure and function: a view of recent progress.Journal of muscle research and cell motility · 2020Review
- Dysregulation of Calcium Handling in Duchenne Muscular Dystrophy-Associated Dilated Cardiomyopathy: Mechanisms and Experimental Therapeutic Strategies.Journal of clinical medicine · 2020Review
- Pressure Overload Is Associated With Low Levels of Troponin I and Myosin Binding Protein C Phosphorylation in the Hearts of Patients With Aortic Stenosis.Frontiers in physiology · 2020Article
- Infantile restrictive cardiomyopathy: cTnI-R170G/W impair the interplay of sarcomeric proteins and the integrity of thin filaments.PloS one · 2020Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Contraction in the mammalian heart is controlled by the intracellular Ca(2+) concentration as it is in all striated muscle, but the heart has an additional signaling system that comes into play to increase heart rate and cardiac output during exercise or stress. β-adrenergic stimulation of heart muscle cells leads to release of cyclic-AMP and the activation of protein kinase A which phosphorylates key proteins in the sarcolemma, sarcoplasmic reticulum and contractile apparatus. Troponin I (TnI) and Myosin Binding Protein C (MyBP-C) are the prime targets in the myofilaments. TnI phosphorylation lowers myofibrillar Ca(2+)-sensitivity and increases the speed of Ca(2+)-dissociation and relaxation (lusitropic effect). Recent studies have shown that this relationship between Ca(2+)-sensitivity and TnI phosphorylation may be unstable. In familial cardiomyopathies, both dilated and hypertrophic (DCM and HCM), a mutation in one of the proteins of the thin filament often results in the loss of the relationship (uncoupling) and blunting of the lusitropic response. For familial dilated cardiomyopathy in thin filament proteins it has been proposed that this uncoupling is causative of the phenotype. Uncoupling has also been found in human heart tissue from patients with hypertrophic obstructive cardiomyopathy as a secondary effect. Recently, it has been found that Ca(2+)-sensitizing drugs can promote uncoupling, whilst one Ca(2+)-desensitizing drug Epigallocatechin 3-Gallate (EGCG) can reverse uncoupling. We will discuss recent findings about the role of uncoupling in the development of cardiomyopathies and the molecular mechanism of the process.
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Registered trials
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