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Figure 9 | Critical Care

Figure 9

From: β1-adrenoceptor stimulation promotes LPS-induced cardiomyocyte apoptosis through activating PKA and enhancing CaMKII and IκBα phosphorylation

Figure 9

Proposed signaling mechanisms for lipopolysaccharide (LPS)-induced cardiomyocyte apoptosis enhanced by β1 -AR activation. Cardiomyocyte β1-AR activation augments IκBα phosphorylation and TNF-α expression, activates protein kinase A (PKA), enhances calmodulin-dependent protein kinase II (CaMKII) phosphorylation, and subsequently promotes LPS-induced cardiomyocyte apoptosis. Cardiomyocyte PKA activation enhances p38 mitogen-activated protein kinase (MAPK) and c-jun NH2-terminal kinase (JNK) phosphorylation, reduces Bcl-2 protein levels, and in turn leads to an increase in cytochrome c release and caspase-9 activity during LPS challenge.

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Critical Care

ISSN: 1364-8535