Please use this identifier to cite or link to this item: http://hdl.handle.net/1942/42643
Title: Sodium as an Important Regulator of Immunometabolism
Authors: Miyauchi, Hidetaka
Geisberger, Sabrina
Luft, Friedrich C.
Wilck, Nicola
Stegbauer, Johannes
Wiig, Helge
Dechend, Ralf
Jantsch, Jonathan
KLEINEWIETFELD, Markus 
Kempa, Stefan
Mueller, Dominik N.
Issue Date: 2024
Publisher: LIPPINCOTT WILLIAMS & WILKINS
Source: HYPERTENSION, 81 (3) , p. 426 -435
Abstract: Salt sensitivity concerns blood pressure alterations after a change in salt intake (sodium chloride). The heart is a pump, and vessels are tubes; sodium can affect both. A high salt intake increases cardiac output, promotes vascular dysfunction and capillary rarefaction, and chronically leads to increased systemic vascular resistance. More recent findings suggest that sodium also acts as an important second messenger regulating energy metabolism and cellular functions. Besides endothelial cells and fibroblasts, sodium also affects innate and adaptive immunometabolism, immune cell function, and influences certain microbes and microbiota-derived metabolites. We propose the idea that the definition of salt sensitivity should be expanded beyond high blood pressure to cellular and molecular salt sensitivity.
Notes: Müller, DN (corresponding author), Helmholtz Assoc, Max Delbruck Ctr Mol Med, Lindenberger Weg 80, D-13125 Berlin, Germany.
Keywords: macrophages;mitochondria;salts;sodium;T lymphocytes
Document URI: http://hdl.handle.net/1942/42643
ISSN: 0194-911X
e-ISSN: 1524-4563
DOI: 10.1161/HYPERTENSIONAHA.123.19489
ISI #: 001161867700026
Rights: 2023 The Authors. Hypertension is published on behalf of the American Heart Association, Inc., by Wolters Kluwer Health, Inc. This is an open access article under the terms of the Creative Commons Attribution Non-Commercial-NoDerivs License, which permits use, distribution, and reproduction in any medium, provided that the original work is properly cited, the use is noncommercial, and no modifications or adaptations are made.
Category: A1
Type: Journal Contribution
Appears in Collections:Research publications

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