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Curr Pharm Des. 2015;21(4):431-48.

Targeting cardiomyocyte Ca2+ homeostasis in heart failure.

Author information

1
Institute for Experimental Medical Research, Kirkeveien 166, 4.etg. Bygg 7, Oslo University Hospital Ullevål, 0407 Oslo, Norway. w.e.louch@medisin.uio.no.

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.

PMID:
25483944
PMCID:
PMC4475738
[Indexed for MEDLINE]
Free PMC Article

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