ArticleJACC. Basic to translational science2026
Left Ventricular Structural, Physiological, and Transcriptomic Abnormalities in a Novel Porcine Hypertrophic Cardiomyopathy Model.
Article in JACC. Basic to translational science, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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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.
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Who cites it
1 citing paper in PubMed.
- Model Matters: Genetic Architecture and Cardiovascular Physiology in Translational Medicine.JACC. Basic to translational science · 2026Article
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Authors and funding
21 authors.
Funding
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Abstract
Hypertrophic cardiomyopathy (HCM) is a disease of heart muscle commonly caused by variants in genes encoding sarcomere-associated proteins. The mechanisms by which these variants lead to the phenotype are uncertain, partly because of the lack of model systems amenable to integrated translational studies. We generated Yucatan minipigs with heterozygous knockin of the human HCM R403Q variant in MYH7. MYH7 R403Q pigs exhibited hypertrophy similar to humans on cardiac imaging. Relative to wild-type, MYH7 R403Q pigs showed increased interstitial fibrosis, increased myocyte disarray, lower capillary density, and intimal hyperplasia of intramyocardial arterioles with decreased luminal diameters. Bulk RNA sequencing and single nuclear RNA sequencing analyses showed upregulation of profibrotic and proinflammatory pathways. MYH7 R403Q hearts showed hypercontractility, elevated end-diastolic pressures, blunted β-adrenergic enhancement of systolic and diastolic function, and increased Ca
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