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Chen Xiong, Hang Yu, Rong Luo, Wei Kantchev, Yun Hana
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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