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Letter: Critical role of TLR4/FAK signaling pathway in sepsis

 
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Correspondence 
dx.doi.org/10.18081/2333-5106/016-1/7-10
American Journal of BioMedicine Volume 4, Issue 1, pages 7-10
Received November 03, 2015; accepted December 11, 2015; published January 10, 2016 

 Chen Xiong, Hang Yu, Rong Luo, Wei Kantchev, Yun Hanamail of corresponding author

To the Editor:

Han Y et al, wrote an interesting article regarding the crosstalk TLR4/FAK with myocardial suppression after endotoxemia. Despite advances in critical care medicine and use of anti-sepsis therapy, the mortality remains high and the long term outcome is poor for patients that survive sepsis. The severe reality suggests a need for additional therapies to the conventional approach to sepsis, thus, there is an urgent need for effective and safe drugs for the treatment of myocardial sepsis. Toll-like receptor 4 (TLR4) contributes to sepsis pathogenesis and cardiac dysfunction with high mortality in animal model of experimental sepsis. However, the mechanism of TLR4 in sepsis-induced myocardial dysfunction remains unclear. This article will highlight the critical TLR4-mediated sepsis via modulate FAK signaling pathway that lead to pro-inflammatory responses consequences in the myocardial tissue damage.

Keywords: TLR4; FAK; Myocardial dysfunction; Sepsis

Copyright © 2016 by The American Society for BioMedicine and BM-Publisher, Inc.

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