ArticleFrontiers in cardiovascular medicine2022
Rare Genetic Variants Associated With Myocardial Fibrosis: Multi-Ethnic Study of Atherosclerosis.
Article in Frontiers in cardiovascular medicine, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
What it found
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Who cites it
6 citing papers in PubMed, 9 citations in OpenAlex.
- Revolutionizing cardiac fibrosis treatment: the potential of personalized CAR T-cell therapy.Cardio-oncology (London, England) · 2025Review
- A case report of MYH7 mutation-induced restrictive cardiomyopathy.European heart journal. Case reports · 2025Article
- Cardiac Fibrosis in the Multi-Omics Era: Implications for Heart Failure.Circulation research · 2025Review
- Myocardial Fibrosis and Cardiomyopathy Risk: A Genetic Link in the MESA.Circulation. Heart failure · 2023Article
- Association of cardiac troponin T and growth differentiation factor 15 with replacement and interstitial cardiac fibrosis in community dwelling adults: The multi-ethnic study of atherosclerosis.Frontiers in cardiovascular medicine · 2023Article
- Histopathological insights into mitral valve prolapse-induced fibrosis.Frontiers in cardiovascular medicine · 2023Review
Corrections and comments
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Authors and funding
13 authors at 8 institutions in 1 country.
Funding
Abstract
Background: Rare pathogenic variants in cardiomyopathy (CM) genes can predispose to cardiac remodeling or fibrosis. We studied the carrier status for such variants in adults without clinical cardiovascular disease (CVD) in whom cardiac MRI (CMR)-derived measures of myocardial fibrosis were obtained in the Multi-Ethnic Study of Atherosclerosis (MESA). Objectives: To identify CM-associated pathogenic variants and assess their relative prevalence in participants with extensive myocardial fibrosis by CMR. Methods: MESA whole-genome sequencing data was evaluated to capture variants in CM-associated genes ( Results: A total of 1,135 MESA participants had available genetic data and phenotypic measures and were free of clinical CVD at the time of CMR. We identified 6,349 rare variants in CM-associated genes in the overall MESA population, of which six pathogenic/likely pathogenic (P/LP) variants were present in the phenotyped subpopulation. The genes harboring P/LP variants in the case group were Conclusions: We observed a higher prevalence of rare potentially pathogenic CM associated genetic variants in participants with significant myocardial fibrosis quantified in CMR as compared to controls without significant fibrosis. No cardiac structural or functional differences were found between participants with or without P/LP variants.
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