Studies in mouse models of hypertrophic cardiomyopathy have provided insights into the biophysical and biochemical properties of mutated contractile proteins to improve clinical diagnosis and management.
Mouse models of hypertrophic cardiomyopathy provide insights into the biophysical and biochemical properties of mutated contractile proteins, which may translate into improved clinical therapeutics.
Hypertrophic cardiomyopathy (HCM) is a common inherited heart disease with serious adverse outcomes, including heart failure, arrhythmias, and sudden cardiac death. The discovery that mutations in sarcomere protein genes cause HCM has enabled the development of mouse models that recapitulate clinical manifestations of disease. Studies in these models have provided unexpected insights into the biophysical and biochemical properties of mutated contractile proteins and may help to improve clinical diagnosis and management of patients with HCM.
Teekakirikul et al. (Mon,) conducted a review in Hypertrophic cardiomyopathy. Studies in mouse models of hypertrophic cardiomyopathy have provided insights into the biophysical and biochemical properties of mutated contractile proteins to improve clinical diagnosis and management.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: