Advanced glycation end products and their receptor in age-related, non-communicable chronic inflammatory diseases; Overview of clinical evidence and potential contributions to disease

Reynaert, Niki L.; Gopal, Poornima; Rutten, Erica P.A.; Wouters, Emiel F.M.; Schalkwijk, Casper G.

doi:10.1016/j.biocel.2016.06.016

Cited by 96 publications

(75 citation statements)

References 245 publications

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“…(31) The binding of AGEs to their receptor has been reported to induce the expression of inflammatory cytokines, thereby contributing to the progress of age-related diseases. (32) TBE inhibits glycation of a-crystallin in vitro. (18) Furthermore, lutein exhibits antioxidative activity and protects the crystalline lens from cataractogenesis.…”

Section: Discussionmentioning

confidence: 99%

<i>Trapa bispinosa</i> Roxb. and lutein ameliorate cataract in type 1 diabetic rats

Kinoshita

Sugawa

Nanri

et al. 2020

J. Clin. Biochem. Nutr.

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Trapa bispinosa Roxb. is an annual aquatic grass of the citrus family. Although its hot water extract displays antioxidative activity in vitro, little is known about its biological effectiveness. In the present study, we evaluated the extract's inhibitory effect on diabetic cataractogenesis and formation of advanced glycation end product. Lutein, which is beneficial for eye diseases, was administered concurrently. For short term administration, Trapa bispinosa Roxb. hot water extract and/or lutein were admin istered to type 1 diabetic rats. N ε (carboxymethyl)lysine and N ε (carboxyethyl)lysine were quantified in serum using mass spectrometry. The long term administration study was similar to the short term, except that the dosages were lower. In the short term study, co administration of the extract and lutein inhibited N ε (carboxymethyl)lysine and N ε (carboxyethyl)lysine in serum. However, in the long term study, only lutein inhibited N ε (carboxymethyl)lysine and N e (carboxyethyl)lysine in serum. These results suggest that lutein exerts its long term effect regardless of the concentration administered, while the extract exerts its effect when its concentration is increased. Relative to the consumption of the control diet, oral intake of the combination of the extract and lutein significantly inhibited the progression of cataracto genesis in the lens of diabetic rats, even at low doses, and the combination was more effective than individual treatments.

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Section: Discussionmentioning

confidence: 99%

<i>Trapa bispinosa</i> Roxb. and lutein ameliorate cataract in type 1 diabetic rats

Kinoshita

Sugawa

Nanri

et al. 2020

J. Clin. Biochem. Nutr.

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“…The receptor ligand-binding portion is the extracellular V-type domain, while the cytoplasmic tail is necessary for signal transduction as well as adaptor protein association. RAGE has been identified in two extracellular secreted forms: an endogenous secretory (es) form and a soluble (s) form [15]. Even if the sRAGE isoforms are missing transmembrane and cytoplasmic domains, they maintain their ligand-binding ability, acting as decoy receptors and inhibiting the binding between RAGE with their ligands or with other receptors [16]; consequently, sRAGE treatment causes a downregulation of RAGE signaling, thus decreasing inflammation [17].…”

Section: Ragementioning

confidence: 99%

Alarmins in Osteoporosis, RAGE, IL-1, and IL-33 Pathways: A Literature Review

et al. 2020

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Alarmins are endogenous mediators released by cells following insults or cell death to alert the host’s innate immune system of a situation of danger or harm. Many of these, such as high-mobility group box-1 and 2 (HMGB1, HMGB2) and S100 (calgranulin proteins), act through RAGE (receptor for advanced glycation end products), whereas the IL-1 and IL-33 cytokines bind the IL-1 receptors type I and II, and the cellular receptor ST2, respectively. The alarmin family and their signal pathways share many similarities of cellular and tissue localization, functions, and involvement in various physiological processes and inflammatory diseases including osteoporosis. The aim of the review was to evaluate the role of alarmins in osteoporosis. A bibliographic search of the published scientific literature regarding the role of alarmins in osteoporosis was organized independently by two researchers in the following scientific databases: Pubmed, Scopus, and Web of Science. The keywords used were combined as follows: “alarmins and osteoporosis”, “RAGE and osteoporosis”, “HMGB1 and osteoporosis”, “IL-1 and osteoporosis”, “IL 33 and osteopororsis”, “S100s protein and osteoporosis”. The information was summarized and organized in the present review. We highlight the emerging roles of alarmins in various bone remodeling processes involved in the onset and development of osteoporosis, as well as their potential role as biomarkers of osteoporosis severity and progression. Findings of the research suggest a potential use of alarmins as pharmacological targets in future therapeutic strategies aimed at preventing bone loss and fragility fractures induced by aging and inflammatory diseases.

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“…Upon the binding of AGEs with RAGE, oxidative stress levels in cells increase and various cytokines are secreted through the activation of nuclear factor κB (NF-κB), which cause an inflammatory response that results in injury [28,29]. Targeting the AGE-RAGE system may be a novel strategy for diabetic complication therapy.…”

Section: Introductionmentioning

confidence: 99%

Interleukin-10 Protects Schwann Cells against Advanced Glycation End Products-Induced Apoptosis via NF-κB Suppression

Bao²,

Men

et al. 2019

Exp Clin Endocrinol Diabetes

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Demyelination resulting from Schwann cell injury is a main pathological feature of diabetic neuropathy, and a key contributor to this process may be inflammation due to advanced glycation end products (AGEs). Therefore, protection by anti-inflammation agents is anticipated. In this study, we showed that interleukin-10 (IL-10), an anti-inflammatory cytokine, inhibits apoptosis of Schwann cells induced by AGEs in vitro. We isolated and cultured Schwann cells from rat sciatic nerves. As detected by flow cytometry, apoptosis of Schwann cells markedly increased following incubation with AGEs for 48 h. However, pretreatment with IL-10 inhibited AGE-induced apoptosis. The effect of IL-10 on NF-κB, which is a very important regulator of inflammation, was also evaluated, and results showed high levels of phospho-NF-κB and nuclear localization of NF-κB in cells incubated with AGEs but low levels of phospho-NF-κB and cytoplasmic localization in the cells incubated with IL-10, indicating the activation of NF-κB by AGEs and inhibition of NF-κB by IL-10. Moreover, incubating Schwann cells with an NF-κB inhibitor (caffeic acid phenethyl ester) for 30 min before adding AGEs mimicked IL-10, lowering the amount of reactive oxygen species and activity of caspase-3 and also decreasing apoptosis in Schwann cells. These results indicate that IL-10 may protect Schwann cells against AGE-induced apoptosis by attenuating oxidative stress via the inhibition of activation of NF-κB.

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Advanced glycation end products and their receptor in age-related, non-communicable chronic inflammatory diseases; Overview of clinical evidence and potential contributions to disease

Cited by 96 publications

References 245 publications

<i>Trapa bispinosa</i> Roxb. and lutein ameliorate cataract in type 1 diabetic rats

<i>Trapa bispinosa</i> Roxb. and lutein ameliorate cataract in type 1 diabetic rats

Alarmins in Osteoporosis, RAGE, IL-1, and IL-33 Pathways: A Literature Review

Interleukin-10 Protects Schwann Cells against Advanced Glycation End Products-Induced Apoptosis via NF-κB Suppression

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