NDLI: [Ligands of RAGE-Proteins: Role in Intercellular Communication and Pathogenesis of Inflammation].

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[Ligands of RAGE-Proteins: Role in Intercellular Communication and Pathogenesis of Inflammation].

Content Provider	Semantic Scholar
Author	Uspenskaya, Yu A. Komleva, Yu K. Pozhilenkova, Elena Salmin, Vladimir Lopatina, Olga L. Fursov, Andriy Lavrentiev, P. V. Belova, O. A. Salmina, Alla
Copyright Year	2015
Abstract	The review contains data on the diversity of endogenous ligands of RAGE receptors (receptor for advanced glycation end products) that play an important role in the signal transduction in (patho) physiological conditions. RAGE takes part in various physiological processes like cell growth and survival, apoptosis and regeneration. They serve as regulators of inflammatory reactions due to their ability to induce secretion of cytokines and chemokines. In addition, they facilitate elimination of apoptotic cells and mediate innate immune response. We discuss mechanisms of soluble RAGE production as well as the role of membrane and soluble forms of the receptor in cell signaling. Several endogenous ligands of RA GE are well-known: advanced glycation end products (AGE), amyloid-beta (Aβ), nuclear high mobility group box 1 proteins (HMGB1), and calcium-binding proteins S100A4, S100A8/A9, S100A12 u S100B. The review is focused on the mechanisms of the ligands production, their secretion from the cells of various origin, interaction with RAGE, and associated intracellular signal transduction pathways. Special attention is paid to the role of RAGE in pathogenesis of inflammation, particularly, in brain injury and neurodegeneration.
Starting Page	694
Ending Page	703
Page Count	10
File Format	PDF HTM / HTML
DOI	10.15690/vramn566
PubMed reference number	27093797
Journal	Medline
Volume Number	6
Alternate Webpage(s)	https://vestnikramn.spr-journal.ru/jour/article/download/566/549
Alternate Webpage(s)	https://doi.org/10.15690/vramn566
Journal	Vestnik Rossiiskoi akademii meditsinskikh nauk
Language	English
Access Restriction	Open
Content Type	Text
Resource Type	Article

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