Desmin disorganisation: A key feature in feline hypertrophic cardiomyopathy

Wan-Ching Cheng1, Charlotte Lawson2, Lois Wilkie1

  • 1Department of Clinical Science and Services, Royal Veterinary College, Hatfield, Hertfordshire, United Kingdom.

Plos One
|July 14, 2025
PubMed

Insights

Hypertrophic cardiomyopathy (HCM) in cats shows similar subcellular changes as in humans, including protein aggregates and disorganization of cardiomyocyte connections. This suggests a shared cellular response to HCM across species.

Area of Science:

  • Veterinary Pathology
  • Cardiovascular Research
  • Cell Biology

Background:

  • Hypertrophic cardiomyopathy (HCM) is histologically defined by increased ventricular wall thickness and myocyte disarray.
  • Subcellular alterations in human and rodent HCM involve the intermediate filament cytoskeleton (desmin) and proteins crucial for cardiomyocyte connections (beta-catenin, connexin-43).

Purpose of the Study:

  • To investigate if similar subcellular alterations observed in human and rodent HCM are present in feline HCM samples.
  • To compare the expression and organization of desmin, αB-crystallin, beta-catenin, and connexin-43 in feline HCM.

Main Methods:

  • Histological examination of feline HCM samples.
  • Immunohistochemistry and protein expression analysis to detect desmin, αB-crystallin, beta-catenin, and connexin-43.

Main Results:

  • Feline HCM samples exhibit prominent desmin and αB-crystallin aggregates with increased protein expression.
  • Disorganization of beta-catenin and connexin-43 was observed, with aberrant signals at the lateral cardiomyocyte surfaces.
  • These findings indicate subcellular changes analogous to those seen in human and rodent HCM.

Conclusions:

  • The subcellular response in cardiomyocytes to HCM is conserved between cats and humans.
  • This study highlights shared pathological mechanisms of HCM across species.
  • Findings may inform comparative approaches to HCM research and treatment.

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