ReviewBiophysical reviews2017
Tampering with springs: phosphorylation of titin affecting the mechanical function of cardiomyocytes.
Review in Biophysical reviews, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT05745337 (Improving Outcomes in Atrial Fibrillation Patients Aided by Implantable Cardiac Monitor), which is not on this map. Cited by 54 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.
Improving Outcomes in Atrial Fibrillation Patients Aided by Implantable Cardiac Monitor: Evaluation of Chronic Beta-blocker Use Versus As-needed Pharmacological Rate Control
Who cites it
54 citing papers in PubMed, 88 citations in OpenAlex.
- Diastolic contributors in cardiomyocytes of a cardiometabolic HFpEF-like mouse model.The Journal of general physiology · 2026Article
- Titin Is Present in the Elastic Tethers That Connect Separating Anaphase Chromosomes in Crane-Fly Spermatocytes.Cytoskeleton (Hoboken, N.J.) · 2026Article
- Mechanobiology of the diabetic cardiomyocyte: insulin signaling, titin elasticity, and multiscale mechanical dysfunction.Biophysical reviews · 2026Review
- Mending the Achilles heels of titin in cardiac and musculoskeletal disease.Biophysical reviews · 2026Review
- Skeletal muscle knockout of NAD(P)H oxidase 2 delays the development of isotonic diaphragm fatigue in mice.Free radical biology & medicine · 2025Article
- Chronic and acute mediators of passive viscoelasticity in human skeletal muscle fibres.Experimental physiology · 2025Article
- Preventing hypocontractility-induced fibroblast expansion alleviates dilated cardiomyopathy.Science (New York, N.Y.) · 2025Article
- Spatially resolving how cMyBP-C phosphorylation and haploinsufficiency in porcine and human myofibrils affect β-cardiac myosin activity.The Journal of general physiology · 2025Article
- Aerobic and resistance exercise-regulated phosphoproteome and acetylproteome modifications in human skeletal muscle.Nature communications · 2025Article
- Differential sex-dependent susceptibility to diastolic dysfunction and arrhythmia in cardiomyocytes from obese diabetic heart failure with preserved ejection fraction model.Cardiovascular research · 2025Article
- Fatiguing exercise reduces cellular passive Young's modulus in human vastus lateralis muscle.Experimental physiology · 2024Article
- The selective serotonin reuptake inhibitor paroxetine improves right ventricular systolic function in experimental pulmonary hypertension.Journal of molecular and cellular cardiology plus · 2024Article
- Titin: roles in cardiac function and diseases.Frontiers in physiology · 2024Review
- Structural evidence for elastic tethers connecting separating chromosomes in crane-fly spermatocytes.Life science alliance · 2023Article
- Lower heart rates and beta-blockers are associated with new-onset atrial fibrillation.International journal of cardiology. Cardiovascular risk and prevention · 2023Article
- Role of Coxsackievirus B3-Induced Immune Responses in the Transition from Myocarditis to Dilated Cardiomyopathy and Heart Failure.International journal of molecular sciences · 2023Review
- Eccentric muscle contractions: from single muscle fibre to whole muscle mechanics.Pflugers Archiv : European journal of physiology · 2023Review
- Signaling network model of cardiomyocyte morphological changes in familial cardiomyopathy.Journal of molecular and cellular cardiology · 2023Article
- Alterations in cytoskeletal and CaFrontiers in cardiovascular medicine · 2023Article
- Cardiac Sarcomere Signaling in Health and Disease.International journal of molecular sciences · 2022Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Reversible post-translational modifications of various cardiac proteins regulate the mechanical properties of the cardiomyocytes and thus modulate the contractile performance of the heart. The giant protein titin forms a continuous filament network in the sarcomeres of striated muscle cells, where it determines passive tension development and modulates active contraction. These mechanical properties of titin are altered through post-translational modifications, particularly phosphorylation. Titin contains hundreds of potential phosphorylation sites, the functional relevance of which is only beginning to emerge. Here, we provide a state-of-the-art summary of the phosphorylation sites in titin, with a particular focus on the elastic titin spring segment. We discuss how phosphorylation at specific amino acids can reduce or increase the stretch-induced spring force of titin, depending on where the spring region is phosphorylated. We also review which protein kinases phosphorylate titin and how this phosphorylation affects titin-based passive tension in cardiomyocytes. A comprehensive overview is provided of studies that have measured altered titin phosphorylation and titin-based passive tension in myocardial samples from human heart failure patients and animal models of heart disease. As our understanding of the broader implications of phosphorylation in titin progresses, this knowledge could be used to design targeted interventions aimed at reducing pathologically increased titin stiffness in patients with stiff hearts.
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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.