ReviewCardiovascular research2015
Research priorities in sarcomeric cardiomyopathies.
Review in Cardiovascular research, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers, 1 of them a synthesis that pooled it.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
32 citing papers in PubMed, 1 synthesis or guideline pooled it, 52 citations in OpenAlex.
- Cardiomyopathy phenotypes in human-induced pluripotent stem cell-derived cardiomyocytes-a systematic review.Pflugers Archiv : European journal of physiology · 2019Pooled it
- Effect of trimetazidine dihydrochloride therapy on myocardial external efficiency in pre-clinical individuals with a hypertrophic cardiomyopathy pathogenic variant: results of the ENERGY trial.Cardiovascular research · 2025Trial
- Perinatal death in pig models of hypertrophic cardiomyopathy carrying sarcomere pathogenic variants.Journal of molecular and cellular cardiology plus · 2025Article
- Pathogenic genes and clinical prognosis in hypertrophic cardiomyopathy.World journal of cardiology · 2025Review
- Cardiac Sarcomere Signaling in Health and Disease.International journal of molecular sciences · 2022Review
- Modeling hypertrophic cardiomyopathy with human cardiomyocytes derived from induced pluripotent stem cells.Stem cell research & therapy · 2022Review
- Protein haploinsufficiency drivers identify MYBPC3 variants that cause hypertrophic cardiomyopathy.The Journal of biological chemistry · 2021Article
- Differences in molecular phenotype in mouse and human hypertrophic cardiomyopathy.Scientific reports · 2021Article
- Mechanosignaling pathways alter muscle structure and function by post-translational modification of existing sarcomeric proteins to optimize energy usage.Journal of muscle research and cell motility · 2021Article
- Assessment of dynamic cardiac repolarization and contractility in patients with hypertrophic cardiomyopathy.PloS one · 2021Article
- Modelling sarcomeric cardiomyopathies with human cardiomyocytes derived from induced pluripotent stem cells.The Journal of physiology · 2020Review
- Altered C10 domain in cardiac myosin binding protein-C results in hypertrophic cardiomyopathy.Cardiovascular research · 2019Article
- Hypertrophic cardiomyopathy: genetics and clinical perspectives.Cardiovascular diagnosis and therapy · 2019Review
- Unraveling obscurins in heart disease.Pflugers Archiv : European journal of physiology · 2019Review
- Sarcomeric mutations in cardiac diseases.Pflugers Archiv : European journal of physiology · 2019Article
- Extra energy for hearts with a genetic defect: ENERGY trial.Netherlands heart journal : monthly journal of the Netherlands Society of Cardiology and the Netherlands Heart Foundation · 2019Article
- The HCM-causing Y235S cMyBPC mutation accelerates contractile function by altering C1 domain structure.Biochimica et biophysica acta. Molecular basis of disease · 2019Article
- Lost in translation: Interpreting cardiac muscle mechanics data in clinical practice.Archives of biochemistry and biophysics · 2019Review
- Impact of the Myosin Modulator Mavacamten on Force Generation and Cross-Bridge Behavior in a Murine Model of Hypercontractility.Journal of the American Heart Association · 2018Article
- Altered CaFrontiers in physiology · 2018Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 6 institutions in 4 countries.
Funding
Abstract
The clinical variability in patients with sarcomeric cardiomyopathies is striking: a mutation causes cardiomyopathy in one individual, while the identical mutation is harmless in a family member. Moreover, the clinical phenotype varies ranging from asymmetric hypertrophy to severe dilatation of the heart. Identification of a single phenotype-associated disease mechanism would facilitate the design of targeted treatments for patient groups with different clinical phenotypes. However, evidence from both the clinic and basic knowledge of functional and structural properties of the sarcomere argues against a 'one size fits all' therapy for treatment of one clinical phenotype. Meticulous clinical and basic studies are needed to unravel the initial and progressive changes initiated by sarcomere mutations to better understand why mutations in the same gene can lead to such opposing phenotypes. Ultimately, we need to design an 'integrative physiology' approach to fully realize patient/gene-tailored therapy. Expertise within different research fields (cardiology, genetics, cellular biology, physiology, and pharmacology) must be joined to link longitudinal clinical studies with mechanistic insights obtained from molecular and functional studies in novel cardiac muscle systems. New animal models, which reflect both initial and more advanced stages of sarcomeric cardiomyopathy, will also aid in achieving these goals. Here, we discuss current priorities in clinical and preclinical investigation aimed at increasing our understanding of pathophysiological mechanisms leading from mutation to disease. Such information will provide the basis to improve risk stratification and to develop therapies to prevent/rescue cardiac dysfunction and remodelling caused by sarcomere mutations.
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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.