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Review

The Glyoxalase System and Methylglyoxal-Derived Carbonyl Stress in Sepsis: Glycotoxic Aspects of Sepsis Pathophysiology

1
Department of Anesthesiology, Heidelberg University Hospital, 69120 Heidelberg, Germany
2
Department of Medicine I and Clinical Chemistry, Heidelberg University Hospital, 69120 Heidelberg, Germany
*
Author to whom correspondence should be addressed.
Academic Editor: Casper G. Schalkwijk
Int. J. Mol. Sci. 2017, 18(3), 657; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms18030657
Received: 11 February 2017 / Revised: 8 March 2017 / Accepted: 14 March 2017 / Published: 17 March 2017
(This article belongs to the Special Issue Glyoxalase System in Health and Disease 2017)
Sepsis remains one of the leading causes of death in intensive care units. Although sepsis is caused by a viral, fungal or bacterial infection, it is the dysregulated generalized host response that ultimately leads to severe dysfunction of multiple organs and death. The concomitant profound metabolic changes are characterized by hyperglycemia, insulin resistance, and profound transformations of the intracellular energy supply in both peripheral and immune cells. A further hallmark of the early phases of sepsis is a massive formation of reactive oxygen (ROS; e.g., superoxide) as well as nitrogen (RNS; e.g., nitric oxide) species. Reactive carbonyl species (RCS) form a third crucial group of highly reactive metabolites, which until today have been not the focus of interest in sepsis. However, we previously showed in a prospective observational clinical trial that patients suffering from septic shock are characterized by significant methylglyoxal (MG)-derived carbonyl stress, with the glyoxalase system being downregulated in peripheral blood mononuclear cells. In this review, we give a detailed insight into the current state of research regarding the metabolic changes that entail an increased MG-production in septicemia. Thus, we point out the special role of the glyoxalase system in the context of sepsis. View Full-Text
Keywords: sepsis; septic shock; metabolic stress; immunometabolism; Warburg effect; reactive carbonyl species; methylglyoxal; glyoxalase sepsis; septic shock; metabolic stress; immunometabolism; Warburg effect; reactive carbonyl species; methylglyoxal; glyoxalase
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MDPI and ACS Style

Schmoch, T.; Uhle, F.; Siegler, B.H.; Fleming, T.; Morgenstern, J.; Nawroth, P.P.; Weigand, M.A.; Brenner, T. The Glyoxalase System and Methylglyoxal-Derived Carbonyl Stress in Sepsis: Glycotoxic Aspects of Sepsis Pathophysiology. Int. J. Mol. Sci. 2017, 18, 657. https://0-doi-org.brum.beds.ac.uk/10.3390/ijms18030657

AMA Style

Schmoch T, Uhle F, Siegler BH, Fleming T, Morgenstern J, Nawroth PP, Weigand MA, Brenner T. The Glyoxalase System and Methylglyoxal-Derived Carbonyl Stress in Sepsis: Glycotoxic Aspects of Sepsis Pathophysiology. International Journal of Molecular Sciences. 2017; 18(3):657. https://0-doi-org.brum.beds.ac.uk/10.3390/ijms18030657

Chicago/Turabian Style

Schmoch, Thomas, Florian Uhle, Benedikt H. Siegler, Thomas Fleming, Jakob Morgenstern, Peter P. Nawroth, Markus A. Weigand, and Thorsten Brenner. 2017. "The Glyoxalase System and Methylglyoxal-Derived Carbonyl Stress in Sepsis: Glycotoxic Aspects of Sepsis Pathophysiology" International Journal of Molecular Sciences 18, no. 3: 657. https://0-doi-org.brum.beds.ac.uk/10.3390/ijms18030657

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