The Receptor for Advanced Glycation Endproducts (RAGE) Contributes to Severe Inflammatory Liver Injury in Mice
Toni Weinhage; Timo Wirth; Paula Schütz; P. Scott Becker; Aloys Lueken; Boris V. Skryabin; Helmut Wittkowski; Dirk Foell · 2020 · Frontiers in Immunology
WASTE classifies this as Negative / Null Result Report · AI classification, approximate
The study found no significant effect — useful as a negative control or null benchmark for your own design.
Abstract
Background. The receptor for advanced glycation end products (RAGE) is a multiligand receptor involved in a number of processes and disorders. While it is known that RAGE-signaling can contribute to toxic liver damage and fibrosis, its role in acute inflammatory liver injury and septic multiorgan failure is yet undefined. We examined RAGE in lipopolysaccharide (LPS) induced acute liver injury of D-galN sensitized mice as a classical model for tumor necrosis factor alpha (TNF-α) dependent inflammatory organ damage. Methods. Mice (Rage-/- and C57BL/6) were intraperitoneally injected with D galN
Abstract by Toni Weinhage; Timo Wirth; Paula Schütz; P. Scott Becker; Aloys Lueken; Boris V. Skryabin; Helmut Wittkowski; Dirk Foell, Frontiers in Immunology (2020) — licensed CC BY 4.0.
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Metadata source: OpenAlex · DOI 10.3389/fimmu.2020.01157
