# Molecular Cardiac Changes in Feline Hyperthyroidism and Hypertrophic Cardiomyopathy: Focus on Desmin, Calreticulin, and Interleukin-10 Expression

## TL;DR

This study examines heart changes in cats with hyperthyroidism and HCM, focusing on proteins like desmin and interleukin-10 to understand shared cardiac injury pathways.

## Contribution

The study identifies shared molecular changes in hyperthyroidism and HCM in cats, particularly in desmin and interleukin-10 expression.

## Key findings

- Hyperthyroid cats showed similar desmin loss and interleukin-10 increase as HCM-affected cats.
- These changes were linked to cardiomyocyte degeneration and coronary artery narrowing.
- Protein alterations occurred despite no significant difference in left ventricular dimensions.

## Abstract

Hyperthyroidism is an important endocrine disorder in adult and old cats, affecting multiple organs, with the heart developing a hypertrophic cardiomyopathy phenotype. Cardiac hypertrophy may resolve with treatment, but structural alterations persist. This study was conducted to assess the changes in proteins present in healthy and affected myocardium and based on left ventricular specimens obtained from cats with hyperthyroidism, hypertrophic cardiomyopathy, and from healthy cats. The immunohistochemical analysis presented both hyperthyroidism and hypertrophic cardiomyopathy groups with a significant loss of contractile protein (desmin) and an increase in interleukin-10, a cytokine characterised by anti-inflammatory properties and activated in myocardial remodelling. These changes were mainly related to cardiomyocyte degeneration and narrowing of the coronary arteries, and not to the primary disease.

Feline hyperthyroidism is the most frequent endocrinopathy in adult and senior cats, frequently leading to cardiac changes characterised by a hypertrophic cardiomyopathy (HCM) phenotype, which may partially reverse with appropriate treatment. However, the structural and molecular alterations in the myocardium can persist and closely resemble those observed in hypertrophic cardiomyopathy. Despite this clinical overlap, protein expression patterns in the hearts of hyperthyroid cats remain poorly understood. This study aimed to evaluate the myocardial expression of desmin, a key contractile protein, as well as calreticulin and interleukin-10 proteins involved in cardiac remodelling and response to injury. Left ventricular samples were obtained from 16 hyperthyroid cats, 12 cats with HCM, and 10 healthy controls. Immunohistochemical staining was performed to assess the expression patterns of the selected proteins. Our findings revealed that, despite median left ventricular dimensions not being significantly different from ones observed in healthy animals, cats with hyperthyroidism exhibited similar alterations in desmin and interleukin-10 expression to those seen in HCM-affected cats. These changes were associated with cardiomyocyte degeneration and coronary artery narrowing, suggesting a shared pathway of myocardial injury independent of the primary disease.