ArticleJournal of cardiovascular translational research2024
Novel Genetic Variants Associated with Primary Myocardial Fibrosis in Sudden Cardiac Death Victims.
Article in Journal of cardiovascular translational research, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed.
- Postmortem genetic testing in sudden death: clinical and medico-legal implications.International journal of legal medicine · 2026Article
- Runx1 drives cardiac fibrosis and heart failure through epigenetic activation of myofibroblasts in pressure overload-induced cardiac remodeling.BMC cardiovascular disorders · 2025Article
- Revolutionizing cardiac fibrosis treatment: the potential of personalized CAR T-cell therapy.Cardio-oncology (London, England) · 2025Review
- Cardiac Fibrosis in the Multi-Omics Era: Implications for Heart Failure.Circulation research · 2025Review
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Authors and funding
13 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Myocardial fibrosis is a common finding in victims of sudden cardiac death (SCD). Whole exome sequencing was performed in 127 victims of SCD with primary myocardial fibrosis as the only pathological finding. These cases are derived from the Fingesture study which has collected data from autopsy-verified SCD victims in Northern Finland. A computational approach was used to identify protein interactions in cardiomyocytes. Associations of the identified variants with cardiac disease endpoints were investigated in the Finnish national genetic study (FinnGen) dataset. We identified 21 missense and one nonsense variant. Four variants were estimated to affect protein function, significantly associated with SCD/primary myocardial fibrosis (Fingesture) and associated with cardiac diseases in Finnish population (FinnGen). These variants locate in cartilage acidic protein 1 (CRATC1), calpain 1 (CAPN1), unc-45 myosin chaperone A (UNC45A) and unc-45 myosin chaperone B (UNC45B). The variants identified contribute to function of extracellular matrix and cardiomyocytes.
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Registered trials
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