alexa Aquaporins in Sepsis
ISSN: 2471-2663

Clinical & Medical Biochemistry
Open Access

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Aquaporins in Sepsis

Katharina Rump* and Michael Adamzik

Clinic for Anaesthesiology, Intensive Care and Pain Therapy, University Hospital Knappschaftskrankenhaus Bochum-Langendreer, Ruhr-University Bochum, Bochum, Germany

*Corresponding Author:
Katharina Rump
Clinic for Anesthesiology, Intensive Care and Pain Therapy
University Hospital Knappschaftskrankenhaus Bochum- Langendreer
In der Schornau 55, D-45882 Bochum, D-45882 Bochum, Germany
Tel: (+49) (234) 32-29242
Fax: (+49) (234) 299-3009
E-mail: [email protected]

Received date: May 17, 2017; Accepted date: May 27, 2017; Published date: June 10, 2017

Citation: Rump K, Adamzik M (2017) Aquaporins in Sepsis. Clin Med Biochem 3:126. doi:10.4172/2471-2663.1000126

Copyright: © 2017 Rump K, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

 

Abstract

Sepsis is a common cause of death in intensive care units worldwide. Due to the high complexity of this immunological syndrome development of novel therapeutic strategies is urgent. Promising drug targets or biomarkers may depict aquaporins (AQPs) as they regulate several key mechanisms of sepsis. Here we report on base of the current literature that several AQPs are involved in different physiological processes of sepsis. In immune system, mainly AQPs 3, 5 and 9 seem to be important, as they regulate the migration of different immune cells. Several studies showed that AQP3 is essential for T-cell function and macrophage migration and that AQP5 and AQP9 regulate neutrophil cell migration and impact sepsis survival. Additionally, to the function in immune system AQPs 1 and 5 play a role in sepsis induced lung injury and their downregulation after inflammatory stimulus impair lung injury. By contrast, AQP4 expression is up-regulated during brain inflammation and aggravates brain edema in sepsis. In kidney AQP2 expression is downregulated in sepsis and can cause renal failure. Some studies also suggest a role of AQP1 in cardiac function. In conclusion AQPs are involved in many physiological dysfunctions in sepsis and their expressions are differently regulated. For development of successful therapeutic strategies, more research on genetic regulatory mechanisms of AQPs is needed.

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