ArticleMedical research archives2024
Dilated Cardiomyopathy - Exploring the Underlying Causes.
Article in Medical research archives, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 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
5 citing papers in PubMed.
- AI-Enabled Sensor Technologies for Remote Arrhythmic Monitoring in High-Risk Cardiomyopathy Genotypes.Sensors (Basel, Switzerland) · 2026Review
- A song of heads and tails: myosin II conformational regulation and filament dynamics shape force generation in non-muscle cells.Biophysical reviews · 2026Review
- Molecular Pathology of Cardiomyopathies: Bridging Morphology, Genomics, and Clinical Phenotypes.Current issues in molecular biology · 2026Review
- New Biomarkers in the Diagnosis and Prognosis of Dilated Cardiomyopathy: Pro-Resolving Lipids and miRNAs.Cells · 2025Article
- Cardiomyopathies and a brief insight into DOX-induced cardiomyopathy.The Egyptian heart journal : (EHJ) : official bulletin of the Egyptian Society of Cardiology · 2025Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
1 author.
Funding
Abstract
Cardiovascular disease is one of the world's leading causes of natural mortality, taking approximately 18 million lives each year. Dilated cardiomyopathy, a subgroup of cardiac diseases, has an annual incidence of 5 - 8 cases per 100,000 for European and North American populations. Common features of dilated cardiomyopathy include cardiac chamber enlargement, impaired systolic function, reduced ejection fraction, and arrhythmias, with an endpoint of ventricular dilation and heart failure. The focus of this paper is to review the non-genetic and genetic etiologies that lead to dilated cardiomyopathy. The non-genetic causes of dilated cardiomyopathy that are discussed include viruses, cardiotoxicity, recreational drugs, and chemotherapeutic medications. For the genes that lead to dilated cardiomyopathy, the focus of this paper is on cytoskeletal and sarcomeric protein genes. Our scope in defining this area will be to explore numerous mouse models that incorporate mutations found in humans that lead to dilated cardiomyopathy. The purpose of the paper is to define the morphological and physiological consequences of these mutations and how this information has furthered our understanding of the disease. Having gained invaluable knowledge from these animal models, it is hoped that new and improved therapeutic approaches can be developed for the treatment and prevention of dilated cardiomyopathy.
Identifiers
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.