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Abstract
An extensive network of regulation of systemic inflammation makes development of a reproducible experimental model of sepsis a complex task. There is no single mouse model that can capture all clinical aspects of this complicated pathology. However, a combination of existing approaches can go a long way towards analysis of specific mechanisms of sepsis development and to the design of novel therapeutic approaches. This review describes the popular mouse models of sepsis and septic shock, as well as their limitations and development strategies.
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ACKNOWLEDGMENTS
I am grateful to D.V. Kuprash for careful reading of the manuscript and helpful advice.
Funding
This work was supported by the Program of fundamental research for state academies for 2013–2020 (research topic no. 01201363823).
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Engelhardt Institute of Molecular Biology, Russian Academy of Sciences, 119991, Moscow, Russia
K. V. Korneev
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Translated by T. Tkacheva
Abbreviations: LPS, lipopolysaccharide;D-GalN,D-galactosamine; PRR, pattern recognition receptor; DAMP, damage-associated molecular pattern; CLP, cecal ligation and puncture; CASP, colon ascendens stent peritonitis.
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Korneev, K.V. Mouse Models of Sepsis and Septic Shock.Mol Biol53, 704–717 (2019). https://doi.org/10.1134/S0026893319050108
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