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Targeting Cardiomyocyte Ca2+ Homeostasis in Heart Failure

[ Vol. 21 , Issue. 4 ]

Author(s):

Asmund T. Roe, Michael Frisk and William E. Louch   Pages 431 - 448 ( 18 )

Abstract:


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.

Keywords:

Cardiac myocytes, calcium homeostasis, heart failure, SR Ca2+ ATPase, Na+/Ca2+ exchanger, ryanodine receptor, t-tubules.

Affiliation:

Institute for Experimental Medical Research, Kirkeveien 166, 4.etg. Bygg 7, Oslo University Hospital UllevÄl, 0407 Oslo, Norway.



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