activation of myocardial phosphoinositide-3-kinase p110α ameliorates cardiac dysfunction and improves survival in polymicrobial sepsis激活心肌phosphoinositide-3-kinase p110α改善心脏功能障碍,提高脓毒症生存幼童腹壁薄弱.pdfVIP

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activation of myocardial phosphoinositide-3-kinase p110α ameliorates cardiac dysfunction and improves survival in polymicrobial sepsis激活心肌phosphoinositide-3-kinase p110α改善心脏功能障碍,提高脓毒症生存幼童腹壁薄弱.pdf

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activation of myocardial phosphoinositide-3-kinase p110α ameliorates cardiac dysfunction and improves survival in polymicrobial sepsis激活心肌phosphoinositide-3-kinase p110α改善心脏功能障碍,提高脓毒症生存幼童腹壁薄弱

Activation of Myocardial Phosphoinositide-3-Kinase p110a Ameliorates Cardiac Dysfunction and Improves Survival in Polymicrobial Sepsis 1 2 1 3 1 4 5 Chuanfu Li , Fang Hua , Tuanzhu Ha , Krishna Singh , Chen Lu , John Kalbfleisch , Kevin F. Breuel , 5 1,2 1 1 1 Tiffany Ford , Race L. Kao , Ming Gao , Tammy R. Ozment , David L. Williams * 1 Department of Surgery, Quillen College of Medicine, East Tennessee State University, Johnson City, Tennessee, United States of America, 2 Department of Emergency Medicine, Emory University School of Medicine Atlanta, Georgia, United States of America, 3 Department of Biomedical Sciences, Quillen College of Medicine, East Tennessee State University, Johnson City, Tennessee, United States of America, 4 Department of Biometry and Medical Computing, Quillen College of Medicine, East Tennessee State University, Johnson City, Tennessee, United States of America, 5 Department of Obstetrics and Gynecology, Quillen College of Medicine, East Tennessee State University, Johnson City, Tennessee, United States of America Abstract 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, p110a (caPI3K Tg). caPI3K Tg and wild type (WT) mice were