ArticleResearch in veterinary science2022
Elevated angiotensin-converting enzyme 2 (ACE2) expression in cats with hypertrophic cardiomyopathy.
Article in Research in veterinary science, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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Who cites it
3 citing papers in PubMed.
- Understanding Pathophysiological Complexity of Feline Hypertrophic Cardiomyopathy Using SWATH-MS Plasma Proteomics.Animals : an open access journal from MDPI · 2026Article
- Clinical-Diagnostic and Therapeutic Advances in Feline Hypertrophic Cardiomyopathy.Veterinary sciences · 2025Review
- Linking clinical and imaging diagnostic assessments of the feline hypertrophic cardiomyopathy phenotype.Frontiers in veterinary science · 2025Review
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Authors and funding
6 authors.
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Abstract
Angiotensin-converting enzyme 2 (ACE2) is an enzyme within the renin-angiotensin-aldosterone system that plays a role in regulating blood pressure. However, it is also a cellular receptor for infection with SARS coronaviruses. Although most cats develop subclinical or mild disease following infection with severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) acquired from human patients, a previous study has suggested hypertrophic cardiomyopathy (HCM) is a potential risk factor for the development of severe disease in the cat. Herein we investigate the ACE2 protein expression in the lung, heart, and kidney from a small subset of cats with (n = 10) and without HCM (n = 10) by immunohistochemistry. The abundance and intensity of ACE2 expression is slightly elevated in alveoli (p = 0.09; 0.07, respectively) and bronchioles (p = 0.095; 0.37, respectively). However, statistically elevated abundance and intensity of ACE-2 expression was only evident in the heart of cats with HCM (p = 0.032; p = 0.011, respectively). Further investigation did not demonstrate a statistical correlation between the ACE2 expression in the heart in relation to the heart weight to body weight ratio, and the ventricular wall ratio. Current findings suggest an overexpression of ACE2 in HCM cases but follow up study is warranted to understand the pathophysiological process.
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