Advanced Glycation End Products research
When glucose reacts non-enzymatically with proteins and lipids over time, it produces a chemically diverse family of molecules known as Advanced Glycation End Products, or AGEs, which accumulate in tissues and drive much of the cellular damage seen in diabetes and aging. Researchers in this area investigate how AGEs and related danger signals like HMGB1 activate the receptor RAGE and toll-like receptors, triggering inflammatory cascades and mitochondrial superoxide production that progressively injure blood vessels, nerves, and kidneys. A central open question is how these overlapping signaling pathways interact at the molecular level — particularly how oxidative stress and inflammation reinforce each other in a self-sustaining cycle that persists even when blood glucose is brought under control. Clarifying these mechanisms could eventually point toward therapeutic targets that interrupt diabetic complications at a much earlier stage than current treatments allow.
- Works
- 47,267
- Total citations
- 1,229,710
- 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↗ 8,995
- Association of glycaemia with macrovascular and microvascular complications of type 2 diabetes (UKPDS 35): prospective observational study↗ 8,966OA
- Neuroinflammation in Alzheimer's disease↗ 5,971OA
- Oxidative Stress and Diabetic Complications↗ 5,354OA
- Normalizing mitochondrial superoxide production blocks three pathways of hyperglycaemic damage↗ 4,251
- Release of chromatin protein HMGB1 by necrotic cells triggers inflammation↗ 4,162
- Vagus nerve stimulation attenuates the systemic inflammatory response to endotoxin↗ 4,117
- 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↗ 3,711
- Targeting the KEAP1-NRF2 System to Prevent Kidney Disease Progression↗ 3,448
- HMG-1 as a Late Mediator of Endotoxin Lethality in Mice↗ 3,384
- 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.