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Cardiac Myosin - DOAJ

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Last Updated: 16 September 2022

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Transcriptome Profile Identifies Actin as an Essential Regulator of Cardiac Myosin Binding Protein C3 Hypertrophic Cardiomyopathy in a Zebrafish Model

Variants in cardiac myosin-binding protein C are the leading cause of inherited hypertrophic cardiomyopathy, with cMyBP-C playing a central role in the core of the nation's contractile machinery. We developed a zebrafish mypbc3-knockout model to investigate the c-MYBPC3-related cardiac disease. The mutants displayed an early cardiac phenotype of myocardium remodeling, concurrent cardiomyocyte hyperplasia, and elevated ejection fractions as early developmental steps in HCM initiation to counteract the increased ventricular myocardial wall strain at the early stages of larval development. In both the mypbc3 heterozygous and homozygous groups, the examination of zebrafish adults revealed a thickened ventricular wall with decreased heart rate, swimming speed, and endurance endurance. In addition, heart transcriptome profiling revealed a significant decline in the actin-filament-based process, indicating an ineffective actin cytoskeleton assembly as the key dysregulating factor associated with the early ventricular cardiac hypertrophy in the zebrafish mypbc3 HCM model.

Source link: https://doi.org/10.3390/ijms23168840

* Please keep in mind that all text is summarized by machine, we do not bear any responsibility, and you should always check original source before taking any actions

* Please keep in mind that all text is summarized by machine, we do not bear any responsibility, and you should always check original source before taking any actions