Pathophysiology of RAGE in inflammatory diseases

Dong, Hanbing; Zhang, Yue; Huang, Yu Chuen; Deng, Hui

doi:10.3389/fimmu.2022.931473

Cited by 92 publications

(54 citation statements)

References 208 publications

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“…The receptor for AGEs (RAGE) is a multi-ligand receptor that has been demonstrated as the important role in the onset and progression of many diseases, such as diabetic complications, cardiovascular diseases, neuropathy, nephropathy, and cancer [ 23 ]. Therefore, AGE-RAGE ligation is the critical event in the progression of aging-related disorders [ 33 ].…”

Section: Discussionmentioning

confidence: 99%

“…A CircuLex AGE-RAGE in vitro Binding Assay Kit (No. CY-8151, MBL Medical & Biological Laboratories Co. Ltd., Nagoya, Japan) was used to determine the inhibitory effects of GKM3- and GKK2-fermented supernatants on RAGE ligation, which is an important biological response in the onset and progression of various diseases [ 23 ]. The assay was carried out according to the manufacturer’s instructions.…”

Section: Methodsmentioning

confidence: 99%

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Fermented Supernatants of Lactobacillus plantarum GKM3 and Bifidobacterium lactis GKK2 Protect against Protein Glycation and Inhibit Glycated Protein Ligation

Lin

Jao

et al. 2023

Nutrients

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With age, protein glycation in organisms increases continuously. Evidence from many studies shows that the accumulation of glycated protein is highly correlated with biological aging and the development of aging-related diseases, so developing a dietary agent to attenuate protein glycation is very meaningful. Previous studies have indicated that lactic acid bacteria-fermented products have diverse biological activities especially in anti-aging, so this study was aimed to investigate the inhibitory effect of the fermented supernatants of Lactobacillus plantarum GKM3 (GKM3) and Bifidobacterium lactis GKK2 (GKK2) on protein glycation. The results show that GKM3- and GKK2-fermented supernatants can significantly inhibit protein glycation by capturing a glycation agent (methylglyoxal) and/or protecting functional groups in protein against methylglyoxal-induced responses. GKM3- and GKK2-fermented supernatants can also significantly inhibit the binding of glycated proteins to the receptor for advanced glycation end products (RAGE). In conclusion, lactic acid bacteria fermentation products have the potential to attenuate biological aging by inhibiting protein glycation.

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Section: Discussionmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

Fermented Supernatants of Lactobacillus plantarum GKM3 and Bifidobacterium lactis GKK2 Protect against Protein Glycation and Inhibit Glycated Protein Ligation

Lin

Jao

et al. 2023

Nutrients

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“…For example, vascularisation that develops after denervation may also lead to the influx of DCs (15). Moreover, in patients with T1D/T2D, increased levels of AGE/RAGE signaling in neurons may induce the activation of inflammatory and oxidative stress pathways, including the NF-kB pathway, potentially causing damage and death of neuronal cells (99)(100)(101).…”

Section: Associations Between Corneal Dcs and Corneal Nervesmentioning

confidence: 99%

Corneal dendritic cells in diabetes mellitus: A narrative review

Liu

Lee

et al. 2023

Front. Endocrinol.

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Diabetes mellitus is a global public health problem with both macrovascular and microvascular complications, such as diabetic corneal neuropathy (DCN). Using in-vivo confocal microscopy, corneal nerve changes in DCN patients can be examined. Additionally, changes in the morphology and quantity of corneal dendritic cells (DCs) in diabetic corneas have also been observed. DCs are bone marrow-derived antigen-presenting cells that serve both immunological and non-immunological roles in human corneas. However, the role and pathogenesis of corneal DC in diabetic corneas have not been well understood. In this article, we provide a comprehensive review of both animal and clinical studies that report changes in DCs, including the DC density, maturation stages, as well as relationships between the corneal DCs, corneal nerves, and corneal epithelium, in diabetic corneas. We have also discussed the associations between the changes in corneal DCs and various clinical or imaging parameters, including age, corneal nerve status, and blood metabolic parameters. Such information would provide valuable insight into the development of diagnostic, preventive, and therapeutic strategies for DM-associated ocular surface complications.

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“…Certainly, binding of AGEs to RAGE initiates intracellular signaling pathways leading to inflammation and oxidative stress which are important part of host–pathogen defense, but can also result in β-cell injury [ 101 , 106 , 108 ]. However, AGE ligation resulting in RAGE signaling is also implicated in many other inflammatory conditions including neurodegenerative conditions, rheumatoid arthritis, and inflammatory bowel disease [ 82 , 98 , 134 , 135 ]. The binding of AGEs to RAGE commonly activates the nuclear factor kappa B (NF-κB) inflammatory pathway and other transcription factors such as mitogen activated protein kinase (MAPK), and Janus kinase (JAK-STAT), increasing the production of proinflammatory cytokines ( Figure 4 ) [ 136 ].…”

Section: Main Textmentioning

confidence: 99%

Advanced Glycation End Products and Inflammation in Type 1 Diabetes Development

Whiddett

Buckle

et al. 2022

Cells

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Type 1 diabetes (T1D) is an autoimmune disease in which the β-cells of the pancreas are attacked by the host’s immune system, ultimately resulting in hyperglycemia. It is a complex multifactorial disease postulated to result from a combination of genetic and environmental factors. In parallel with increasing prevalence of T1D in genetically stable populations, highlighting an environmental component, consumption of advanced glycation end products (AGEs) commonly found in in Western diets has increased significantly over the past decades. AGEs can bind to cell surface receptors including the receptor for advanced glycation end products (RAGE). RAGE has proinflammatory roles including in host–pathogen defense, thereby influencing immune cell behavior and can activate and cause proliferation of immune cells such as islet infiltrating CD8+ and CD4+ T cells and suppress the activity of T regulatory cells, contributing to β-cell injury and hyperglycemia. Insights from studies of individuals at risk of T1D have demonstrated that progression to symptomatic onset and diagnosis can vary, ranging from months to years, providing a window of opportunity for prevention strategies. Interaction between AGEs and RAGE is believed to be a major environmental risk factor for T1D and targeting the AGE-RAGE axis may act as a potential therapeutic strategy for T1D prevention.

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Pathophysiology of RAGE in inflammatory diseases

Cited by 92 publications

References 208 publications

Fermented Supernatants of Lactobacillus plantarum GKM3 and Bifidobacterium lactis GKK2 Protect against Protein Glycation and Inhibit Glycated Protein Ligation

Fermented Supernatants of Lactobacillus plantarum GKM3 and Bifidobacterium lactis GKK2 Protect against Protein Glycation and Inhibit Glycated Protein Ligation

Corneal dendritic cells in diabetes mellitus: A narrative review

Advanced Glycation End Products and Inflammation in Type 1 Diabetes Development

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