title: Targeting cardiomyocyte Ca2+ homeostasis in heart failure.
abstract: Improved treatments for heart failure patients will require the development of novel therapeutic strategies that target basal disease mechanisms. Disrupted cardiomyocyte Ca(2+) homeostasis is recognized as a major contributor to the heart failure phenotype, as it plays a key role in systolic and diastolic dysfunction, arrhythmogenesis, and hypertrophy and apoptosis signaling. In this review, we outline existing knowledge of the involvement of Ca(2+) homeostasis in these deficits, and identify four promising targets for therapeutic intervention: the sarcoplasmic reticulum Ca(2+) ATPase, the Na(+)-Ca(2+) exchanger, the ryanodine receptor, and t-tubule structure. We discuss experimental data indicating the applicability of these targets that has led to recent and ongoing clinical trials, and suggest future therapeutic approaches.
authors.forename: Asmund T
authors.initials: AT
authors.lastname: Roe
authors.forename: Michael
authors.initials: M
authors.lastname: Frisk
authors.affiliation: Institute for Experimental Medical Research, Kirkeveien 166, 4.etg. Bygg 7, Oslo University Hospital Ullevål, 0407 Oslo, Norway. w.e.louch@medisin.uio.no.
authors.forename: William E
authors.initials: WE
authors.lastname: Louch
mesh_terms: D002118:Calcium / Q000378:metabolism*; D006333:Heart Failure / Q000188:drug therapy* / Q000378:metabolism; D006706:Homeostasis / Q000187:drug effects*; D006801:Humans; D032383:Myocytes, Cardiac / Q000187:drug effects* / Q000378:metabolism
chemical_list: D002118:Calcium