ReviewCell metabolism2015
The genetic landscape of cardiomyopathy and its role in heart failure.
Review in Cell metabolism, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 78 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
78 citing papers in PubMed, 133 citations in OpenAlex.
- Impact of Genetic Testing for Cardiomyopathy on Emotional Well-Being and Family Dynamics: A Study of Parents and Adolescents.Circulation. Genomic and precision medicine · 2021Trial
- Characterization of Dystrophin-Related Syndromes: Carriers, DMD, and BMD.Muscles (Basel, Switzerland) · 2026Review
- The Role of Next-Generation Sequencing in the Management of Asymptomatic, Young Slovenian Athletes for Distinction Between Athlete's Heart and Cardiomyopathy.Biomedicines · 2026Article
- Missense variants in the myosin binding domains ofbioRxiv : the preprint server for biology · 2025Article
- Investigating the dual role of mitochondrial and nuclear genome variants in pediatric cardiomyopathies.Scientific reports · 2025Article
- Myosin relaxation states in skeletal muscle fibers of rats and mice: Effects of sex and adiposity.Physiological reports · 2025Article
- Vinculin haploinsufficiency impairs integrin-mediated costamere remodeling on stiffer microenvironments.Journal of molecular and cellular cardiology · 2025Article
- Duality in disease: How two amino acid substitutions at actin residue 312 result in opposing forms of cardiomyopathy.The Journal of biological chemistry · 2024Article
- Structural dynamics of the intrinsically disordered linker region of cardiac troponin T.bioRxiv : the preprint server for biology · 2024Article
- Precision Genetic Therapies: Balancing Risk and Benefit in Patients with Heart Failure.Current cardiology reports · 2024Review
- Review
- Knockdown of SCN5A alters metabolic-associated genes and aggravates hypertrophy in the cardiomyoblast.Molecular biology reports · 2024Article
- Article
- Fine tuning contractility: atrial sarcomere function in health and disease.American journal of physiology. Heart and circulatory physiology · 2024Review
- Harnessing human genetics and stem cells for precision cardiovascular medicine.Cell genomics · 2024Review
- Recessive TMOD1 mutation causes childhood cardiomyopathy.Communications biology · 2024Article
- Case Report: Lethal mitochondrial cardiomyopathy linked to a compound heterozygous variant ofFrontiers in cardiovascular medicine · 2024Article
- Unraveling the mystery of oligogenic inheritance under way?Molecules and cells · 2024Article
- High prevalence ofFrontiers in cardiovascular medicine · 2024Article
- Hypertrophic cardiomyopathy inThe journal of cardiovascular aging · 2024Article
18 more citing papers are in PubMed but not listed here.
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
Heart failure is highly influenced by heritability, and nearly 100 genes link to familial cardiomyopathy. Despite the marked genetic diversity that underlies these complex cardiovascular phenotypes, several key genes and pathways have emerged. Hypertrophic cardiomyopathy is characterized by increased contractility and a greater energetic cost of cardiac output. Dilated cardiomyopathy is often triggered by mutations that disrupt the giant protein titin. The energetic consequences of these mutations offer molecular targets and opportunities for new drug development and gene correction therapies.
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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.