Impaired myosin isoform shift and calcium transients contribute to cellular pathogenesis of rat cirrhotic cardiomyopathy.
Hooman HonarHongqun LiuMei L ZhangTamara K GlennHenk E D J Ter KeursSamuel S LeePublished in: Liver international : official journal of the International Association for the Study of the Liver (2020)
Cardiomyocytes and ventricular trabeculae in a cirrhotic rat model showed features of typical heart failure including systolic and diastolic prolongation, impaired force-frequency relation and decreased force-generating capacity. Impaired myosin isoform shift and calcium transients are important contributory mechanisms underlying the pathogenesis of the heart failure phenotype seen in cirrhosis.