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Review
. 2019 Oct 29;20(21):5376.
doi: 10.3390/ijms20215376.

The Pathogenesis of Sepsis and Potential Therapeutic Targets

Min Huang  1   2 , Shaoli Cai  3   4 , Jingqian Su  5   6
Affiliations
Review

The Pathogenesis of Sepsis and Potential Therapeutic Targets

Min Huang et al. Int J Mol Sci. .

Abstract

Sepsis is defined as "a life-threatening organ dysfunction caused by a host's dysfunctional response to infection". Although the treatment of sepsis has developed rapidly in the past few years, sepsis incidence and mortality in clinical treatment is still climbing. Moreover, because of the diverse manifestations of sepsis, clinicians continue to face severe challenges in the diagnosis, treatment, and management of patients with sepsis. Here, we review the recent development in our understanding regarding the cellular pathogenesis and the target of clinical diagnosis of sepsis, with the goal of enhancing the current understanding of sepsis. The present state of research on targeted therapeutic drugs is also elaborated upon to provide information for the treatment of sepsis.

Keywords: biomarkers; pathogenesis; sepsis; therapeutic drugs.

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Conflict of interest statement

The authors have declared no conflict of interest.

Figures

Figure 1
Figure 1
The complex pathogenesis of sepsis.
Figure 2
Figure 2
The regulation mechanisms of mitochondrial damage during sepsis.
Figure 3
Figure 3
The function of the cholinergic anti-inflammatory pathway (CAP) in sepsis.
Figure 4
Figure 4
Blocking Programmed Death Receptor-1 and Programmed Death Ligand-1 (PD-1/PD-L1) signaling reverses the immunosuppression in sepsis.
See this image and copyright information in PMC

References

    1. Rocheteau P., Chatre L., Briand D., Mebarki M., Jouvion G., Bardon J., Crochemore C., Serrani P., Lecci P.P., Latil M., et al. Sepsis induces long-term metabolic and mitochondrial muscle stem cell dysfunction amenable by mesenchymal stem cell therapy. Nat. Commun. 2015;6:10145. doi: 10.1038/ncomms10145. - DOI - PMC - PubMed
    1. Paoli C.J., Reynolds M.A., Sinha M., Gitlin M., Crouser E. Epidemiology and Costs of Sepsis in the United States-An Analysis Based on Timing of Diagnosis and Severity Level. Crit. Care Med. 2018;46:1889–1897. doi: 10.1097/CCM.0000000000003342. - DOI - PMC - PubMed
    1. Iwashyna T.J., Cooke C.R., Wunsch H., Kahn J.M. Population burden of long-term survivorship after severe sepsis in older Americans. J. Am. Geriatr. Soc. 2012;60:1070–1077. doi: 10.1111/j.1532-5415.2012.03989.x. - DOI - PMC - PubMed
    1. Gaieski D.F., Edwards J.M., Kallan M.J., Carr B.G. Benchmarking the incidence and mortality of severe sepsis in the United States. Crit Care Med. 2013;41:1167–1174. doi: 10.1097/CCM.0b013e31827c09f8. - DOI - PubMed
    1. Barie P.S. World Sepsis Day: September 13, 2012. Surg. Infect. (Larchmt) 2012;13:185–186. doi: 10.1089/sur.2012.9905. - DOI - PubMed