Open veterinary journal · 2025
Myocardial expression of connexin 43 in cats with hypertrophic and restrictive cardiomyopathy phenotype.
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Oleynikov Dmitrij
Аннотация
BACKGROUND: In humans and cats hypertrophic cardiomyopathy (HCM) is a cause of sudden cardiac death. This is usually associated with arrhythmias, based on myocardial fibrosis and electric impulse propagation disturbances. Restrictive cardiomyopathy (RCM) is a CM associated with excessive fibrosis which is predisposed to arrhythmic episodes. Electric coupling in the myocardium is based on the His-Purkinje system and cardiomyocytes cell-to-cell contacts. Cell connection is based on gap junctions and their structural proteins-connexins. Today there is a lack of information in the literature regarding these functional units and their distribution in cats.
AIM: Discover the presence of connexin43 (Cx43) in myocardial tissues of cats and to differentiate in HCM and RCM phenotypes.
METHODS: Retrospective analysis of materials collected from cats with CM.
RESULTS: Animals with the histological animals with histological and immunohistochemical markers of HCM and RCM. Cx43 was distributed in the myocardial tissue of a healthy cat in a typical pattern to other described animals (rats, mice, and human). In HCM, Cx43 was decreased and lateralized near the fibrotic zones, and it was absent in the scar tissue. In RCM, there was a similar pattern, but loci with spontaneously altered expression of Cx43 were also observed, forming lacunas in the gap junction or presented as an intermittent granulated mass.
CONCLUSION: Cx43 has different expression patterns in different CM phenotypes; however, the role of this fact in arrhythmogenesis needs to be studied.
AIM: Discover the presence of connexin43 (Cx43) in myocardial tissues of cats and to differentiate in HCM and RCM phenotypes.
METHODS: Retrospective analysis of materials collected from cats with CM.
RESULTS: Animals with the histological animals with histological and immunohistochemical markers of HCM and RCM. Cx43 was distributed in the myocardial tissue of a healthy cat in a typical pattern to other described animals (rats, mice, and human). In HCM, Cx43 was decreased and lateralized near the fibrotic zones, and it was absent in the scar tissue. In RCM, there was a similar pattern, but loci with spontaneously altered expression of Cx43 were also observed, forming lacunas in the gap junction or presented as an intermittent granulated mass.
CONCLUSION: Cx43 has different expression patterns in different CM phenotypes; however, the role of this fact in arrhythmogenesis needs to be studied.