Advanced Glycation End Products research
When glucose reacts non-enzymatically with proteins and lipids over time, it generates a chemically diverse family of molecules called Advanced Glycation End Products, or AGEs, whose accumulation drives much of the tissue damage seen in diabetes and aging. Researchers in this area work to understand how AGEs and related danger signals—particularly the protein HMGB1—activate receptors such as RAGE and Toll-like receptors to trigger oxidative stress and chronic inflammation, with mitochondrial superoxide production emerging as a key amplifier of that damage cascade. A central open question is how these interconnected pathways interact across different cell types and organs to produce the spectrum of diabetic complications, from neuropathy to cardiovascular disease. Active investigation is also focused on whether blocking specific nodes in the AGE–RAGE–HMGB1 axis can interrupt disease progression without disrupting the normal signaling functions these molecules serve.
- Works
- 47,579
- Total citations
- 1,238,876
- Keywords
- Advanced Glycation End ProductsHMGB1Oxidative StressInflammationRAGEDiabetes
Top papers in Advanced Glycation End Products research
Ordered by total citation count.
- Biochemistry and molecular cell biology of diabetic complications↗ 9,037
- Association of glycaemia with macrovascular and microvascular complications of type 2 diabetes (UKPDS 35): prospective observational study↗ 9,027OA
- Neuroinflammation in Alzheimer's disease↗ 6,087OA
- Oxidative Stress and Diabetic Complications↗ 5,397OA
- Normalizing mitochondrial superoxide production blocks three pathways of hyperglycaemic damage↗ 4,264
- Release of chromatin protein HMGB1 by necrotic cells triggers inflammation↗ 4,178
- Vagus nerve stimulation attenuates the systemic inflammatory response to endotoxin↗ 4,144
- Dietary Advanced Glycation End Products and Their Potential Role in Cardiometabolic Disease in Children↗ 4,018OA
- Role of Oxidative Stress in Development of Complications in Diabetes↗ 3,714
- Targeting the KEAP1-NRF2 System to Prevent Kidney Disease Progression↗ 3,451
- HMG-1 as a Late Mediator of Endotoxin Lethality in Mice↗ 3,391
- Resveratrol Reduces the Proinflammatory Effects and Lipopolysaccharide- Induced Expression of HMGB1 and TLR4 in RAW264.7 Cells↗ 3,256OA
Active researchers
Top authors in this area, ranked by h-index.