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- W2669257435 endingPage "1392" @default.
- W2669257435 startingPage "1375" @default.
- W2669257435 abstract "Cardiomyopathies represent a heterogeneous group of diseases that negatively affect heart function. Primary cardiomyopathies specifically target the myocardium, and may arise from genetic [hypertrophic cardiomyopathy (HCM), arrhythmogenic right ventricular cardiomyopathy/dysplasia (ARVC/D), mitochondrial cardiomyopathy] or genetic and acquired [dilated cardiomyopathy (DCM), restrictive cardiomyopathy (RCM)] etiology. Modern genomics has identified mutations that are common in these populations, while in vitro and in vivo experimentation with these mutations have provided invaluable insight into the molecular mechanisms native to these diseases. For example, increased myosin heavy chain (MHC) binding and ATP utilization lead to the hypercontractile sarcomere in HCM, while abnormal protein–protein interaction and impaired Ca2+ flux underlie the relaxed sarcomere of DCM. Furthermore, expanded access to genetic testing has facilitated identification of potential risk factors that appear through inheritance and manifest sometimes only in the advanced stages of the disease. In this review, we discuss the genetic and molecular abnormalities unique to and shared between these primary cardiomyopathies and discuss some of the important advances made using more traditional basic science experimentation." @default.
- W2669257435 created "2017-06-30" @default.
- W2669257435 creator A5019669093 @default.
- W2669257435 creator A5028042700 @default.
- W2669257435 creator A5043449669 @default.
- W2669257435 date "2017-06-23" @default.
- W2669257435 modified "2023-10-16" @default.
- W2669257435 title "Molecular mechanisms in cardiomyopathy" @default.
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