Asmund T. Roe, Michael Frisk and William E. Louch Pages 431 - 448 ( 18 )
Improved treatments for heart failure patients will require the development of novel therapeutic strategies that target basal disease mechanisms. Disrupted cardiomyocyte Ca2+ 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 Ca2+ homeostasis in these deficits, and identify four promising targets for therapeutic intervention: the sarcoplasmic reticulum Ca2+ ATPase, the Na+-Ca2+ 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.
Cardiac myocytes, calcium homeostasis, heart failure, SR Ca<sup>2+</sup> ATPase, Na<sup>+</sup>/Ca<sup>2+</sup> exchanger, ryanodine receptor, t-tubules.
, , Institute for Experimental Medical Research, Kirkeveien 166, 4.etg. Bygg 7, Oslo University Hospital Ullevål, 0407 Oslo, Norway.