Year: 2015
Type: review
Abstract: To date, no compounds or interventions exist that treat or prevent sarcomeric cardiomyopathies. Established therapies currently improve the outcome, but novel therapies may be able to more fundamentally affect the disease process and course. Investigations of the pathomechanisms are generating molecular insights that can be useful for the design of novel specific drugs suitable for clinical use. As perturbations in the heart are stage-specific, proper timing of drug treatment is essential to prevent initiation and progression of cardiac disease in mutation carrier individuals. In this review, we emphasize potential novel therapies which may prevent, delay, or even reverse hypertrophic cardiomyopathy caused by sarcomeric gene mutations. These include corrections of genetic defects, altered sarcomere function, perturbations in intracellular ion homeostasis, and impaired myocardial energetics.
Source: Cardiovascular Research
DOI: 10.1093/cvr/cvv023
Institutions: University of Arizona, University Medical Center Hamburg-Eppendorf, German Centre for Cardiovascular Research, University of California, Davis, University of Florence, University Hospital Regensburg, University of Oxford, Vanderbilt University Medical Center, Netherlands Heart Institute, Amsterdam Cardiovascular Sciences, Amsterdam UMC Location Vrije Universiteit Amsterdam
Language: English
Subfield: Cardiology and Cardiovascular Medicine
Field: Medicine
Domain: Health Sciences
Open Access status: bronze
Funders: Gilead Sciences, Deutsches Zentrum für Herz-Kreislaufforschung, British Heart Foundation, European Commission, Deutsche Forschungsgemeinschaft, Fondation Leducq, Bundesministerium für Bildung und Forschung, Nederlandse Organisatie voor Wetenschappelijk Onderzoek, National Institutes of Health, Medical Research Council, National Heart, Lung, and Blood Institute
Awards: G1438367337, CaMKII and InsP3-Mediated Signaling in Cardiac Myocytes, G2179780285, G2546053586, G3071622502, G3300645866, G573276430, Bench-to-beside Integrated approach to familial hypertrophic cardiomyopathy: to the HEART of the disease, The interaction of myosin and the thin filament: how mutations cause allosteric dysfunction and their connection to genetic cardiomyopathy, Ionic Control of Cardiac Muscle Contraction: EC Coupling, G7373811569, Integrative Approach to Divergent Remodeling in Thin Filament Cardiomyopathies
OpenAlex ID: W2123552783