ReviewCirculation research2019
Novel Therapies for Prevention and Early Treatment of Cardiomyopathies.
Review in Circulation research, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers, 1 of them a synthesis that pooled it.
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
42 citing papers in PubMed, 1 synthesis or guideline pooled it, 69 citations in OpenAlex.
- A multiancestry polygenic risk score improves stratification in patients with hypertrophic cardiomyopathy.Nature cardiovascular research · 2026Pooled it
- 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
- Case Report: A typical triad of Danon disease caused by a LAMP2 splice-donor variant with multilevel functional validation.Frontiers in cardiovascular medicine · 2026Article
- Rethinking Childhood-Onset Hypertrophic Cardiomyopathy: A Review of Molecular Mechanisms and Unique Therapy Considerations.Journal of cardiovascular development and disease · 2025Review
- Role and research progress of histone modification in cardiovascular diseases (Review).Experimental and therapeutic medicine · 2025Review
- An FDA-approved drug structurally and phenotypically corrects the K210del mutation in genetic cardiomyopathy models.The Journal of clinical investigation · 2025Article
- Endoplasmic reticulum stress in cardiomyopathies: from the unfolded protein response to therapeutic opportunities.Frontiers in cardiovascular medicine · 2025Review
- Metrnl and Cardiomyopathies: From Molecular Mechanisms to Therapeutic Insights.Journal of cellular and molecular medicine · 2025Review
- Natural history and clinical outcomes of patients with hypertrophic cardiomyopathy from thin filament mutations.ESC heart failure · 2024Review
- Review
- Excess long-term risk of adverse outcomes in heart failure patients with high and low levels of NT-proBNP: A 7-year follow-up study (NorthStar Trial).International journal of cardiology. Heart & vasculature · 2024Article
- Frameshift variants in C10orf71 cause dilated cardiomyopathy in human, mouse, and organoid models.The Journal of clinical investigation · 2024Article
- Protein phosphatase 2A anchoring disruptor gene therapy for familial dilated cardiomyopathy.Molecular therapy. Methods & clinical development · 2024Article
- Article
- Review
- AFrontiers in genetics · 2024Article
- Secondary structures that regulate mRNA translation provide insights for ASO-mediated modulation of cardiac hypertrophy.Nature communications · 2023Article
- Regulated cell death pathways in cardiomyopathy.Acta pharmacologica Sinica · 2023Review
- The genetic basis for adult-onset idiopathic dilated cardiomyopathy in people of African descent.Heart failure reviews · 2023Review
- Secondary structures that regulate mRNA translation provide insights for ASO-mediated modulation of cardiac hypertrophy.bioRxiv : the preprint server for biology · 2023Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 2 institutions in 2 countries.
Funding
Abstract
Heritable cardiomyopathies are a class of heart diseases caused by variations in a number of genetic loci. Genetic variants on one allele lead to either a degraded protein, which causes a haploinsufficiency of that protein, or a nonfunctioning protein that subverts the molecular system within which the protein works. Over years, both of these mechanisms eventually lead to diseased heart tissue and symptoms of a failing heart. Most cardiomyopathy treatments repurpose heart failure drugs to manage these symptoms and avoid adverse outcomes. There are few therapies that correct the underlying pathogenic genetic or molecular mechanism. This review will reflect on this unmet clinical need in genetic cardiomyopathies and consider a variety of therapies that address the mechanism of disease rather than patient symptoms. These therapies are genetic, targeting a defective gene or transcript, or ameliorating a genetic insufficiency. However, there are also a number of small molecules under exploration that modulate downstream faulty protein products affected in cardiomyopathies.
Indexed as
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.