ArticleiScience2026
Phenotypic patterns in feline heart failure: A natural model for understanding variable disease severity in humans.
Article in iScience, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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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.
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13 authors.
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Abstract
Cats frequently develop myocardial remodeling, for example, hypertrophic cardiomyopathy, affecting 14.7% of domestic cats compared to 0.2% of humans, with shared genetic features making them relevant to human disease. Yet features distinguishing clinical outcomes such as heart failure and arterial thromboembolism remain poorly characterized. Using artificial-intelligence-based digital pathology and Oxford Nanopore sequencing, we analyzed myocardial tissue from 37 cats grouped by outcome: arterial thromboembolism, congestive heart failure, or no documented cardiac disease. Myocardial fibrosis was significantly higher in cats with arterial thromboembolism, indicating a distinct fibrotic phenotype. Cats with heart failure showed nuclear hypertrophy, while cats with arterial thromboembolism had increased numbers of small, hematoxylin-dense non-myocyte nuclei. Higher fibrosis was associated with downregulation of mitochondrial and cardiac conduction genes, and nuclear size correlated with proteostasis and stress-response pathways. This multimodal framework reveals distinct histological and molecular profiles by outcome, with relevance for translational hypertrophic cardiomyopathy research.
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