ReviewJournal of molecular and cellular cardiology2010
Rescue of familial cardiomyopathies by modifications at the level of sarcomere and Ca2+ fluxes.
Review in Journal of molecular and cellular cardiology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 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
23 citing papers in PubMed, 30 citations in OpenAlex.
- The MYH7 c.2770G > A (p.Glu924Lys) mutation exhibits phenotypic heterogeneity in hypertrophic cardiomyopathy (HCM) and restrictive cardiomyopathy (RCM): a case report.BMC cardiovascular disorders · 2025Article
- Exploration of calcium and amino acids for children with primary cardiomyopathies based on genetic characteristics.Frontiers in pediatrics · 2025Article
- Cellular and extracellular proteomic profiling of paradoxical low-flow low-gradient aortic stenosis myocardium.Frontiers in cardiovascular medicine · 2024Article
- Insulin-like growth factor binding protein 2: a core biomarker of left ventricular dysfunction in dilated cardiomyopathy.Hereditas · 2023Article
- Structures of PKA-phospholamban complexes reveal a mechanism of familial dilated cardiomyopathy.eLife · 2022Article
- Modifications of Sarcoplasmic Reticulum Function Prevent Progression of Sarcomere-Linked Hypertrophic Cardiomyopathy Despite a Persistent Increase in Myofilament Calcium Response.Frontiers in physiology · 2020Article
- Novel Therapies for Prevention and Early Treatment of Cardiomyopathies.Circulation research · 2019Review
- Therapeutic Strategies Targeting Inherited Cardiomyopathies.Current heart failure reports · 2017Review
- Update on hypertrophic cardiomyopathy and a guide to the guidelines.Nature reviews. Cardiology · 2016Review
- N-acetylcysteine reverses diastolic dysfunction and hypertrophy in familial hypertrophic cardiomyopathy.American journal of physiology. Heart and circulatory physiology · 2015Article
- Research priorities in sarcomeric cardiomyopathies.Cardiovascular research · 2015Review
- Mechanistic heterogeneity in contractile properties of α-tropomyosin (TPM1) mutants associated with inherited cardiomyopathies.The Journal of biological chemistry · 2015Article
- Long term ablation of protein kinase A (PKA)-mediated cardiac troponin I phosphorylation leads to excitation-contraction uncoupling and diastolic dysfunction in a knock-in mouse model of hypertrophic cardiomyopathy.The Journal of biological chemistry · 2014Article
- Desensitization of myofilaments to Ca2+ as a therapeutic target for hypertrophic cardiomyopathy with mutations in thin filament proteins.Circulation. Cardiovascular genetics · 2014Article
- Integration of troponin I phosphorylation with cardiac regulatory networks.Circulation research · 2013Review
- Subtle abnormalities in contractile function are an early manifestation of sarcomere mutations in dilated cardiomyopathy.Circulation. Cardiovascular genetics · 2012Article
- Arginylation regulates myofibrils to maintain heart function and prevent dilated cardiomyopathy.Journal of molecular and cellular cardiology · 2012Article
- Myosin binding protein C: implications for signal-transduction.Journal of muscle research and cell motility · 2012Review
- Long-term rescue of a familial hypertrophic cardiomyopathy caused by a mutation in the thin filament protein, tropomyosin, via modulation of a calcium cycling protein.Journal of molecular and cellular cardiology · 2011Article
- Anabolic androgenic steroids and intracellular calcium signaling: a mini review on mechanisms and physiological implications.Mini reviews in medicinal chemistry · 2011Review
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
Abstract
Cardiomyopathies are a heterogeneous group of diseases of the myocardium associated with mechanical and/or electrical dysfunction that frequently show inappropriate ventricular hypertrophy or dilation. Current data suggest that numerous mutations in several genes can cause cardiomyopathies, and the severity of their phenotypes is also influenced by modifier genes. Two major types of inherited cardiomyopathies include familial hypertrophic cardiomyopathy (FHC) and dilated cardiomyopathy (DCM). FHC typically involves increased myofilament Ca(2+) sensitivity associated with diastolic dysfunction, whereas DCM often results in decreased myofilament Ca(2+) sensitivity and systolic dysfunction. Besides alterations in myofilament Ca(2+) sensitivity, alterations in the levels of Ca(2+)-handling proteins have also been described in both diseases. Recent work in animal models has attempted to rescue FHC and DCM via modifications at the myofilament level, altering Ca(2+) homeostasis by targeting Ca(2+)-handling proteins, such as the sarcoplasmic reticulum ATPase and phospholamban, or by interfering with the products of different modifiers genes. Although attempts to rescue cardiomyopathies in animal models have shown great promise, further studies are needed to validate these strategies in order to provide more effective and specific treatments.
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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.