ArticlePloS one2025
Desmin disorganisation: A key feature in feline hypertrophic cardiomyopathy.
Article in PloS one, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
What it found
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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.
- Linoleic Acid and Linolenic Acid May Alleviate Heart Failure Through Aquaporin (AQP1) and Gut Microbiota.Foods (Basel, Switzerland) · 2025Article
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Authors and funding
8 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Hypertrophic cardiomyopathy is usually characterised histologically by increased ventricular wall thickness and myocyte disarray. In human and rodent HCM, subcellular alterations were detected that involve the intermediate filament cytoskeleton (mainly desmin) and proteins that are important for mechanical and electrochemical connection of the cardiomyocytes (beta-catenin and connexin-43, respectively). We demonstrate here that similar changes can be visualised in HCM samples from cats, with prominent desmin and αB-crystallin aggregates that are accompanied by increased expression at the protein level. In addition, there is a disorganisation of beta-catenin and connexin-43, which display additional aberrant signals at the lateral surface of cardiomyocytes. This suggests that the subcellular response in cardiomyocytes to HCM is shared by humans and cats.
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Registered trials
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