Send to

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

Targeting cardiomyocyte Ca2+ homeostasis in heart failure.

Author information

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


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.

[Indexed for MEDLINE]
Free PMC Article

Supplemental Content

Full text links

Icon for Bentham Science Publishers Ltd. Icon for PubMed Central Icon for Norwegian BIBSYS system
Loading ...
Support Center