Related Experiment Video
Updated: Dec 12, 2025

Resolving Water, Proteins, and Lipids from In Vivo Confocal Raman Spectra of Stratum Corneum through a Chemometric Approach
Published on: September 26, 2019
In vivo quantitative analysis of advanced glycation end products in atopic dermatitis-Possible culprit for the
Ji Yeon Hong1, Min Jeong Kim2, Jun Ki Hong2
1Department of Dermatology, Seoul National University Hospital, Seoul, Korea.
Abstract:
Advanced glycation end products (AGEs) interact with the membrane-bound receptor for AGEs (RAGE), consequently amplifying the inflammatory response. Soluble receptor for AGE (sRAGE) and endogenous secretory RAGE (esRAGE) act as decoys for AGE and competitively sequester RAGE ligands, thereby serving a cytoprotective role. Our objective was to investigate AGE expression and their receptors in the serum and skin of patients with atopic dermatitis (AD). In this case-control study, the levels of AGE, sRAGE and esRAGE were measured in the blood samples and corneocytes of 29 adult patients with AD and 12 healthy controls by ELISA. Corneocyte AGE levels increased in the AD group (P = .002). Higher corneocyte AGE levels were observed in the severe AD than in the milder form of AD. No significant difference in serum AGE level was observed in patients with AD and healthy controls. Serum sRAGE markedly decreased in patients with AD (P = .007) and serum esRAGE followed a similar trend. In conclusion, dermal accumulation of AGE in AD may have a role in fuelling skin inflammation. The potential after-effects of reduced neutralizer on systemic risk need further evaluation.
Insights
Advanced glycation end products (AGEs) accumulate in the skin of atopic dermatitis (AD) patients, fueling inflammation. Reduced levels of AGEs
Area of Science:
- Dermatology
- Immunology
- Biochemistry
Background:
- Advanced glycation end products (AGEs) trigger inflammatory responses via the receptor for AGEs (RAGE).
- Soluble RAGE (sRAGE) and endogenous secretory RAGE (esRAGE) act as decoys, mitigating AGE-induced inflammation and offering cytoprotection.
Purpose of the Study:
- To investigate the expression of AGEs and their receptors (RAGE, sRAGE, esRAGE) in the serum and skin of patients with atopic dermatitis (AD).
- To correlate AGE and receptor levels with AD severity.
Main Methods:
- A case-control study involving 29 adult AD patients and 12 healthy controls.
- Quantification of AGE, sRAGE, and esRAGE levels in serum and corneocytes using Enzyme-Linked Immunosorbent Assay (ELISA).
- Comparison of levels between AD patients and controls, and correlation with AD severity.
Main Results:
- Corneocyte AGE levels were significantly elevated in AD patients compared to controls (P = .002).
- Higher corneocyte AGE levels were associated with more severe AD.
- Serum AGE levels showed no significant difference between groups.
- Serum sRAGE levels were markedly decreased in AD patients (P = .007), with a similar trend observed for serum esRAGE.
Conclusions:
- Dermal accumulation of AGEs may contribute to skin inflammation in atopic dermatitis.
- Reduced levels of sRAGE and esRAGE in AD patients suggest a diminished capacity to neutralize AGEs.
- Further research is needed to evaluate the systemic risks associated with reduced AGE neutralizers in AD.

