ReviewArchives of biochemistry and biophysics2019
Troponin I modulation of cardiac performance: Plasticity in the survival switch.
Review in Archives of biochemistry and biophysics, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
16 citing papers in PubMed, 24 citations in OpenAlex.
- Sodium nitrate supplementation prevents beneficial cardiac adaptations to running in female mice with few effects on male hearts.Scientific reports · 2026Article
- Effect of Continuous Lipopolysaccharide Induction on Oxidative Stress and Heart Injury in Weaned Piglets.Veterinary sciences · 2025Article
- Hyperactive mTORC1/4EBP1 signaling dysregulates proteostasis and accelerates cardiac aging.GeroScience · 2025Article
- Reduction in myofilament CaFrontiers in physiology · 2025Article
- Post-translational modifications of vertebrate striated muscle myosin heavy chains.Cytoskeleton (Hoboken, N.J.) · 2024Review
- Focus on cardiac troponin complex: From gene expression to cardiomyopathy.Genes & diseases · 2024Review
- Arg92Leu-cTnT Alters the cTnC-cTnI Interface Disrupting PKA-Mediated Relaxation.Circulation research · 2024Article
- Thin filament regulation of cardiac muscle power output: Implications for targets to improve human failing hearts.The Journal of general physiology · 2023Article
- Extracellular Histone-Induced Protein Kinase C Alpha Activation and Troponin Phosphorylation Is a Potential Mechanism of Cardiac Contractility Depression in Sepsis.International journal of molecular sciences · 2023Article
- Myofilament-associated proteins with intrinsic disorder (MAPIDs) and their resolution by computational modeling.Quarterly reviews of biophysics · 2023Review
- Emerging concepts in heart failure management and treatment: focus on SGLT2 inhibitors in heart failure with preserved ejection fraction.Drugs in context · 2023Review
- Phosphoproteomic Analysis Reveals Downstream PKA Effectors of AKAP Cypher/ZASP in the Pathogenesis of Dilated Cardiomyopathy.Frontiers in cardiovascular medicine · 2021Article
- Improved Cardiac Function and Attenuated Inflammatory Response by Additional Administration of Tirofiban during PCI for ST-Segment Elevation Myocardial Infarction Patients.Evidence-based complementary and alternative medicine : eCAM · 2021Article
- LncRNAs in cardiac hypertrophy: From basic science to clinical application.Journal of cellular and molecular medicine · 2020Review
- Site-specific acetyl-mimetic modification of cardiac troponin I modulates myofilament relaxation and calcium sensitivity.Journal of molecular and cellular cardiology · 2020Article
- Current and Future Directions of Myofilament Regulation.Archives of biochemistry and biophysics · 2019Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 2 institutions in 1 country.
Funding
Abstract
Signaling complexes targeting the myofilament are essential in modulating cardiac performance. A central target of this signaling is cardiac troponin I (cTnI) phosphorylation. This review focuses on cTnI phosphorylation as a model for myofilament signaling, discussing key gaps and future directions towards understanding complex myofilament modulation of cardiac performance. Human heart cTnI is phosphorylated at 14 sites, giving rise to a complex modulatory network of varied functional responses. For example, while classical Ser23/24 phosphorylation mediates accelerated relaxation, protein kinase C phosphorylation of cTnI serves as a brake on contractile function. Additionally, the functional response of cTnI multi-site phosphorylation cannot necessarily be predicted from the response of individual sites alone. These complexities underscore the need for systematically evaluating single and multi-site phosphorylation on myofilament cellular and in vivo contractile function. Ultimately, a complete understanding of these multi-site responses requires work to establish site occupancy and dominance, kinase/phosphatase signaling balance, and the function of adaptive secondary phosphorylation. As cTnI phosphorylation is essential for modulating cardiac performance, future insight into the complex role of cTnI phosphorylation is important to establish sarcomere signaling in the healthy heart as well as identification of novel myofilament targets in the treatment of disease.
Indexed as
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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.