Document Type
Article
Publication Date
9-19-2012
Description
Phosphoinositide-3-kinase (PI3K)/Akt dependent signaling has been shown to improve outcome in sepsis/septic shock. There is also ample evidence that PI3K/Akt dependent signaling plays a crucial role in maintaining normal cardiac function. We hypothesized that PI3K/Akt signaling may ameliorate septic shock by attenuating sepsis-induced cardiac dysfunction. Cardiac function and survival were evaluated in transgenic mice with cardiac myocyte specific expression of constitutively active PI3K isoform, p110α (caPI3K Tg). caPI3K Tg and wild type (WT) mice were subjected to cecal ligation/puncture (CLP) induced sepsis. Wild type CLP mice showed dramatic cardiac dysfunction at 6 hrs. Septic cardiomyopathy was significantly attenuated in caPI3K CLP mice. The time to 100% mortality was 46 hrs in WT CLP mice. In contrast, 80% of the caPI3K mice survived at 46 hrs after CLP (p30 days (p
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This work is licensed under a Creative Commons Attribution 4.0 International License.
Citation Information
Li, Chuanfu; Hua, Fang; Ha, Tuanzhu; Singh, Krishna; Lu, Chen; Kalbfleisch, John; Breuel, Kevin F.; Ford, Tiffany; Kao, Race L.; Gao, Ming; Ozment, Tammy R.; and Williams, David L.. 2012. Activation of Myocardial Phosphoinositide-3-Kinase p110α Ameliorates Cardiac Dysfunction and Improves Survival in Polymicrobial Sepsis. PLoS ONE. Vol.7(9). https://doi.org/10.1371/journal.pone.0044712 PMID: 23028587
Copyright Statement
Copyright: ß 2012 Li et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.