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. 2015 Mar 9;19(1):76. doi: 10.1186/s13054-015-0820-1

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© Wang et al.; licensee BioMed Central. 2015

This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly credited. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.

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Proposed signaling mechanisms for lipopolysaccharide (LPS)-induced cardiomyocyte apoptosis enhanced by β ₁ -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.