Abstract
Sepsis is defined as severe systemic inflammation in response to invading pathogens, or an uncontrolled hyperinflammatory response, as mediated by the release of various proinflammatory mediators. Although some patients may die rapidly from septic shock accompanied by an overwhelming systemic inflammatory response syndrome (SIRS) triggered by a highly virulent pathogen, most patients survive the initial phase of sepsis, showing multiple organ damage days or weeks later. These patients often demonstrate signs of immune suppression accompanied by enhanced inflammation. Sepsis is a result of a complex process; there is interaction of various pathways, such as inflammation, immunity, coagulation, as well as the neuroendocrine system. This treatise is an attempt to provide a summary of several key regulatory mechanisms and to present the currently recognized molecular pathways that are involved in the pathogenesis of sepsis.
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Acknowledgments
This work was supported, in part, by grants from the National Natural Science Foundation (81130035, 81372054, 81071545, 81272089, 81121004), the National Basic Research Program of China (2012CB518102), and the Medical Research Foundation of Chinese PLA (AWS11J008, BWS12J050).
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Yao, YM., Luan, YY., Zhang, QH., Sheng, ZY. (2015). Pathophysiological Aspects of Sepsis: An Overview. In: Mancini, N. (eds) Sepsis. Methods in Molecular Biology, vol 1237. Humana Press, New York, NY. https://doi.org/10.1007/978-1-4939-1776-1_2
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DOI: https://doi.org/10.1007/978-1-4939-1776-1_2
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