Advanced Glycation End Products research

When glucose reacts non-enzymatically with proteins and lipids over time, it produces a chemically diverse family of molecules called Advanced Glycation End Products, or AGEs, which accumulate in tissues and drive much of the cellular damage seen in diabetes and aging. These compounds trigger inflammatory cascades largely by binding to a cell-surface receptor called RAGE, and by amplifying oxidative stress through mitochondrial superoxide production and crosstalk with toll-like receptors and damage-associated signals such as HMGB1. Researchers are working to clarify exactly how these molecular events translate into the vascular, neurological, and renal complications that make diabetes so clinically consequential. Central open questions include how to pharmacologically interrupt RAGE signaling without disrupting its normal physiological roles, and how the interplay between glycation, mitochondrial dysfunction, and innate immune activation might be targeted to slow or reverse established diabetic tissue damage.

Works

47,938

Total citations

1,248,056

Keywords

Advanced Glycation End ProductsHMGB1Oxidative StressInflammationRAGEDiabetes