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Targeting the receptor for advanced glycation end products (RAGE) in type 1 diabetes
Author(s) -
Le Bagge Selena,
Fotheringham Amelia K.,
Leung Sherman S.,
Forbes Josephine M.
Publication year - 2020
Publication title -
medicinal research reviews
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.868
H-Index - 130
eISSN - 1098-1128
pISSN - 0198-6325
DOI - 10.1002/med.21654
Subject(s) - rage (emotion) , glycation , proinflammatory cytokine , receptor , medicine , diabetes mellitus , type 1 diabetes , advanced glycation end product , endocrinology , immunology , chemistry , biology , inflammation , neuroscience
Type 1 diabetes (T1D) is one of the most common chronic diseases manifesting in early life, with the prevalence increasing worldwide at a rate of approximately 3% per annum. The prolonged hyperglycaemia characteristic of T1D upregulates the receptor for advanced glycation end products (RAGE) and accelerates the formation of RAGE ligands, including advanced glycation end products, high‐mobility group protein B1, S100 calcium‐binding proteins, and amyloid‐beta. Interestingly, changes in the expression of RAGE and these ligands are evident in patients before the onset of T1D. RAGE signals via various proinflammatory cascades, resulting in the production of reactive oxygen species and cytokines. A large number of proinflammatory ligands that can signal via RAGE have been implicated in several chronic diseases, including T1D. Therefore, it is unsurprising that RAGE has become a potential therapeutic target for the treatment and prevention of disease. In this review, we will explore how RAGE might be targeted to prevent the development of T1D.