Human Autoimmune Diseases and the AGE-RAGE Axis
This systematic review highlights the role of the AGE-RAGE axis in autoimmune diseases, showing that AGE accumulation and RAGE ligands are associated with disease activity. It discusses how AGE-RAGE signaling amplifies pathways related to inflammation, which may contribute to autoimmune pathologies.
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Why it matters
Understanding the AGE-RAGE axis could provide insights into potential therapeutic targets for autoimmune diseases. However, establishing its role in treatment requires rigorous clinical studies and standardized biomarkers.
What this does not prove
The review notes limited direct evidence connecting the AGE-RAGE axis to specific autoimmune conditions, emphasizing a lack of validated biomarkers.
Next milestone
No next milestone was established from the available source.
Study facts
- Study design
- Systematic review
- Participants / samples
- Not reported
- Randomised
- Not reported
- Controlled
- Not reported
- Primary endpoint met
- Not reported
- Relevant MS type
- Not reported
- Publication date
- 2026-09-22
- Evidence reviewed
- Abstract only
- Regulatory approval
- Not reported
- Research areas
- Other
Original sources
- Primary evidenceAntiglycation approach in selected autoimmune diseases: Where do we stand? ↗DOI: 10.1016/j.redox.2026.104410
Supporting passages (6)
study designThis review summarizes current mechanistic, preclinical, and clinical evidence on the role of the AGE-RAGE axis in selected autoimmune diseases, with a focus on systemic lupus erythematosus, rheumatoid arthritis, type 1 diabetes, psoriasis, and multiple sclerosis.
subjectsThis review summarizes current mechanistic, preclinical, and clinical evidence on the role of the AGE-RAGE axis in selected autoimmune diseases, with a focus on systemic lupus erythematosus, rheumatoid arthritis, type 1 diabetes, psoriasis, and multiple sclerosis.
research categoriesOverall, the AGE-RAGE axis represents a plausible therapeutic target in autoimmunity, but establishing its therapeutic potential will require standardized biomarker panels and well-designed clinical trials.
findingsAGE-RAGE signaling amplifies nuclear factor kappa B (NF-κB), mitogen-activated protein kinase (MAPK), Janus kinase/signal transducer and activator of transcription (JAK/STAT), and reactive oxygen species (ROS)-dependent pathways, promotes pro-inflammatory immune phenotypes, and may contribute to neoepitope generation and epitope spreading.
limitationsAlthough several compounds show promising anti-inflammatory and antiglycation effects in experimental models, autoimmune-specific translational evidence remains limited, and most studies do not include validated AGE/RAGE biomarkers.
publication datePublication date: 2026-09-22
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