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. 2010 Feb 16;121(6):822-30.
doi: 10.1161/CIRCULATIONAHA.109.890954. Epub 2010 Feb 1.

Ca2+ cycling and new therapeutic approaches for heart failure

Anne-Marie Lompré  1 , Roger J Hajjar, Sian E Harding, Evangelia G Kranias, Martin J Lohse, Andrew R Marks
Affiliations

Ca2+ cycling and new therapeutic approaches for heart failure

Anne-Marie Lompré et al. Circulation. .
No abstract available

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Figures

Figure 1
Figure 1. Simplified representation of the main Ca2+ handling mechanisms deregulated in heart failure
Depicted in grey are systems which are either down-regulated or inhibited, and in red the systems which are up-regulated or activated in heart failure. GPCR: G-protein-coupled receptors, Gs: stimulatory G protein, GRKs: G protein Receptor kinases, AC: adenylyl cyclase, PKA: protein kinase A, cAMP: cyclic adenosine monophosphate, PDE4D3: phosdiesterase type D3, ICa: Ca2+ influx through L-type Ca2+ channels, HCN: Hyperpolarization-activated cyclic nucleotide-gated channels, EPAC: Exchange protein directly activated by cAMP, MRP4: multidrug-resistant associated protein 4, NCX: sodium-calcium exchanger, RyR2: ryanodine receptor type 2, CSQ: calsequestrin, HRC: histidine-rich Ca2+ binding protein, HAX-1: HS-1 associated protein X-1, SERCA2a: Sarco/endoplasmic reticulum Ca2+ ATPase type 2a, PLN: phospholamban, PP1: phosphatase type 1, I-1: inhibitor 1 of type 1 phosphatase, SAP: stress-activated protein kinase, JNK: c-Jun NH2-terminal kinase, CaN: calcineurin, NFAT: nuclear factor of activated T-cells, CaMK: Ca2+/calmodulin kinase, HDAC: histone deacetylase, MEF2: myocyte enhancing factor 2. Red dots indicate phosphorylation, red arrows phosphorylation, blue arrows transport and black arrows activation.
See this image and copyright information in PMC

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