Mechanistic Insights into Feline Hypertrophic Cardiomyopathy: Pathway Analysis Highlights Age and Sex Differences
Hypertrophic cardiomyopathy (HCM) is the most common acquired heart disease in cats, mirroring many clinical and pathological features seen in human HCM. Despite its prevalence, the molecular mechanisms driving the disease in felines remain poorly understood. This study delves into the molecular changes occurring in heart muscle cells (cardiomyocytes) in cats affected by HCM to uncover how these alterations contribute to disease development.
Study Design: Focus on Cardiomyocyte Function Markers
Researchers analyzed left ventricular free wall myocardium samples from 15 cats diagnosed with feline HCM (fHCM) and 30 healthy control cats. The control group included two age categories: 16 young cats aged about 18 months and 14 older adult cats without cardiac disease. Using RT-qPCR (reverse transcription quantitative PCR), they measured the expression levels of key molecular markers related to cardiomyocyte function.
Key Findings: Age and Sex Impact Cardiac Gene Expression
Age-Related Expression Patterns: All molecular markers showed highest expression in young healthy cats, with a clear decline as cats aged, independent of sex.
Disease-Associated Changes: Compared to older healthy cats, those with HCM exhibited increased expression of most disease-related markers, indicating ongoing cardiac remodeling or stress.
Sex Differences: Male cats with HCM had higher expression levels of all markers compared to female cats, suggesting sex-specific variations in disease progression and cardiac response.
Continuous Myocardial Adaptation: The presence of marker expression throughout life reflects the heart’s ongoing adaptation to physiological demands, heightened during early life and disease.
Implications for Understanding Feline HCM
This study emphasizes the importance of considering both age and sex when investigating the pathogenesis of feline HCM. The heightened myocardial responsiveness observed in young cats and in males with HCM suggests potential windows for targeted intervention or closer monitoring. Moreover, these findings parallel observations in human cardiomyopathy, strengthening the cat’s role as a relevant model for translational cardiovascular research.
Conclusion
By revealing how cardiomyocyte gene expression varies with age, sex, and disease status, this research advances our understanding of the molecular basis of feline HCM. These insights provide valuable directions for future studies aimed at developing precision treatments for affected cats and improving comparative cardiac medicine.
