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Aging skin in atopic dermatitis - are advanced glycation end products guilty?
( Jun Ki Hong ) , ( Ji Yeon Hong ) , ( Min Jeong Kim ) , ( Su Jung Park ) , ( Kui Young Park ) , ( Seong Jun Seo )
프로그램북 71권 2호 388-388(1pages)
UCI I410-ECN-0102-2021-500-000133936
이 자료는 4페이지 이하의 자료입니다.

Background: Advanced glycation end products (AGEs), the well-known aging biomarker, interact with the membrane-bound receptor for AGEs (RAGE), consequently amplifying inflammatory response. Soluble receptor for AGE (sRAGE) and endogenous secretory RAGE (esRAGE) act as decoy for AGE and competitively sequester RAGE ligands, thereby serving a cytoprotective role. However, there are few studies that discuss their actions in dermatologic fields, especially with atopic dermatitis (AD). Objectives: This study aimed to investigate the expression of AGE and the receptors in serum and skin of AD patients. Methods: Blood samples and corneocytes were taken from 29 adult AD patients and 12 healthy controls. The levels of AGE, sRAGE and esRAGE were evaluated by enzyme-linked immunosorbent assay. Results: Level of cutaneous AGE was elevated in AD group (p=0.002). Severe AD group showed higher skin AGE than milder group. No significant difference was found between AD patients and healthy controls in serum AGE level. Serum sRAGE was markedly decreased in AD patients (p=0.007) and serum esRAGE followed similar trend. Conclusion: Dermal accumulation of AGE in AD may have a role in fueling skin inflammation. The potential effect of reduced neutralizer - serum sRAGE - on metabolic and cardiovascular risk need further evaluation.

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