ReviewFrontiers in cardiovascular medicine2022
Suppression of lusitropy as a disease mechanism in cardiomyopathies.
Review in Frontiers in cardiovascular medicine, 2022. 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
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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
16 citing papers in PubMed, 21 citations in OpenAlex.
- Immature and mature myocardium in the pathophysiology of hypertrophic cardiomyopathy.Journal of molecular and cellular cardiology plus · 2026Review
- Biventricular Impella Support for Ventricular Tachycardia Ablation in a Patient With Severe Dilated Cardiomyopathy.Clinical case reports · 2026Article
- The splice of life: how alternative splicing shapes regulatory and phenotypic evolution.The EMBO journal · 2026Review
- Cardiac Troponin C E135A Variant Impairs Myofilament Response to PKA Phosphorylation and Is Associated With Autosomal Dominant Dilated Cardiomyopathy With Diastolic Dysfunction.Circulation. Genomic and precision medicine · 2025Article
- Effects of Ellagic Acid on Myocardial Contractility in Isolated and Perfused Rat Hearts.Biomedicines · 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
- Time course of cardiovascular responses to acute sustained handgrip exercise in young physically active men.Physiological reports · 2025Article
- Editorial: Physiology of human myopathies.Frontiers in physiology · 2025Article
- Post-translational modifications of vertebrate striated muscle myosin heavy chains.Cytoskeleton (Hoboken, N.J.) · 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
- Nucleus Mechanosensing in Cardiomyocytes.International journal of molecular sciences · 2023Review
- Mouse Models of Cardiomyopathies Caused by Mutations in Troponin C.International journal of molecular sciences · 2023Review
- Phospholamban R14del disease: The past, the present and the future.Frontiers in cardiovascular medicine · 2023Review
- Repurposing Cyclic Guanosine Monophosphate Pathway Medications, from Vasodilation toward Changing the Face of Heart Failure.Heart views : the official journal of the Gulf Heart AssociationArticle
- Clinical pharmacology of cardiac cyclic AMP in human heart failure: too much or too little?Expert review of clinical pharmacologyArticle
Corrections and comments
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Authors and funding
2 authors at 2 institutions in 2 countries.
Funding
Abstract
In cardiac muscle the action of adrenaline on β1 receptors of heart muscle cells is essential to adjust cardiac output to the body's needs. Adrenergic activation leads to enhanced contractility (inotropy), faster heart rate (chronotropy) and faster relaxation (lusitropy), mainly through activation of protein kinase A (PKA). Efficient enhancement of heart output under stress requires all of these responses to work together. Lusitropy is essential for shortening the heartbeat when heart rate increases. It therefore follows that, if the lusitropic response is not present, heart function under stress will be compromised. Current literature suggests that lusitropy is primarily achieved due to PKA phosphorylation of troponin I (TnI) and phospholamban (PLB). It has been well documented that PKA-induced phosphorylation of TnI releases Ca
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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.