Targeting Cardiomyocyte Ca2+ Homeostasis in Heart Failure

Author(s): Asmund T. Roe, Michael Frisk, William E. Louch

Journal Name: Current Pharmaceutical Design

Volume 21 , Issue 4 , 2015

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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.

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Article Details

Year: 2015
Published on: 03 December, 2014
Page: [431 - 448]
Pages: 18
DOI: 10.2174/138161282104141204124129

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