Receptor for Advanced Glycation End Products (RAGE): A Pivotal Hub in Immune Diseases

Abstract

As a critical molecule in the onset and sustainment of inflammatory response, the receptor for advanced glycation end products (RAGE) has a variety of ligands, such as advanced glycation end products (AGEs), S100/calcium granule protein, and high-mobility group protein 1 (HMGB1). Recently, an increasing number studies have shown that RAGE ligand binding can initiate the intracellular signal cascade, affect intracellular signal transduction, stimulate the release of cytokines, and play a vital role in the occurrence and development of immune-related diseases, such as systemic lupus erythematosus, rheumatoid arthritis, and Alzheimer’s disease. In addition, other RAGE signaling pathways can play crucial roles in life activities, such as inflammation, apoptosis, autophagy, and endoplasmic reticulum stress. Therefore, the strategy of targeted intervention in the RAGE signaling pathway may have significant therapeutic potential, attracting increasing attention. In this paper, through the systematic induction and analysis of RAGE-related signaling pathways and their regulatory mechanisms in immune-related diseases, we provide theoretical clues for the follow-up targeted intervention of RAGE-mediated diseases.

Cellular and molecular heterogeneities and signatures, and pathological trajectories of fatal COVID-19 lungs defined by spatial single-cell transcriptome analysis

“…AGER, predominantly expressed in ACs (Fig. 2C), is a multiligand receptor interacting with AGE and other molecules implicated in lung homeostasis, development and inflammation, and certain diseases such as diabetes and Alzheimer's disease, and regulates diverse pathways including MyD88dependent, nuclear receptors, TNF-a, ERK1/2 and p38 MAPK, and p53/TP53 pathways [20][21][22][23]. Following interaction with S100A12, AGER triggers the activation of mononuclear phagocytes, lymphocytes, and endothelium by generating key proinflammatory mediators [24].…”

Effect and mechanism of acupuncture on Alzheimer’s disease: A review

“…In patients with AD, IL-1 is overexpressed in the receptive area of the cerebral cortex, and the concentration in the tissue increases accordingly (Yue et al, 2022). Tang et al (2005) used the method of chemical damage to establish the AD rat model, and selected acupoints: "Dazhui, " "Shenshu, " "Taixi, " and "Housanli" acupoints (Wang et al, 2020c).…”

Corneal dendritic cells in diabetes mellitus: A narrative review

“…There are several pathogeneses involved in the inflammatory state of T2D, including tissue hypoxia, cell death of expanding adipose tissue, activation of interleukins, and nuclear factor (NF)-kB pathways, contributing to the recruitment and activation of immune cells (5,7,64). For example, the NF-kB signaling pathway may be activated via the interaction of advanced glycation end-products (AGEs) and its cognate receptor for advanced glycation end-products (RAGE), subsequently promoting the secretion of TNF-a, IL-1b, IL-6, and other pro-inflammatory cytokines (65)(66)(67)(68). Significantly increased levels of various AGEs compounds have been reported in both type 1 and type 2 diabetic patients, resulting from non-enzymatic glycation and oxidation of proteins and lipids (65,(69)(70)(71)(72)(73)(74)(75).…”