Advanced Glycation End Products (AGEs) contribute to the pathogenesis of numerous chronic diseases through mechanisms such as oxidative stress, inflammation, and protein cross-linking. Below is a structured list of major AGE-associated conditions.
| Disease / Condition | Role of AGEs in Pathogenesis | Notes / Evidence |
| Diabetes Mellitus & Complications | AGEs accumulate due to chronic hyperglycemia, leading to cross-linking of collagen in blood vessels, basement membrane thickening, and microvascular damage. AGEs activate RAGE, amplifying inflammation. | Strongly linked to retinopathy, nephropathy, neuropathy; supported by numerous clinical studies. |
| Cardiovascular Disease | AGE-modified LDL promotes atherosclerotic plaque formation; cross-linked collagen reduces arterial elasticity. Increased oxidative stress promotes endothelial dysfunction. | Elevated serum CML and pentosidine levels correlate with CVD risk. |
| Chronic Kidney Disease | Reduced renal clearance increases circulating AGEs; AGEs further damage glomeruli and promote fibrosis. | Skin autofluorescence and serum AGEs correlate with CKD progression. |
| Neurodegenerative Diseases (Alzheimer’s, Parkinson’s) | AGEs contribute to amyloid-beta aggregation, tau hyperphosphorylation, and neuronal oxidative damage. | Post-mortem brain tissue shows elevated AGE-modified proteins in Alzheimer’s. |
| Osteoporosis & Bone Fragility | Pentosidine and other AGEs cross-link collagen in bone, reducing toughness and increasing brittleness. | High pentosidine levels are predictive of fracture risk. |
| Skin Aging | AGEs cross-link dermal collagen and elastin, reducing elasticity and leading to wrinkles. | UV exposure accelerates AGE formation in skin. |
| Diabetic Wound Healing Impairment | AGE-modified extracellular matrix proteins impair fibroblast migration and angiogenesis. | AGE accumulation in wound tissue delays closure and increases infection risk. |
| Respiratory Diseases (COPD, Asthma) | Tobacco smoke is a rich exogenous source of AGEs; RAGE activation promotes airway inflammation. | Higher AGE burden found in COPD patient lung tissue. |
| Cancer | AGE–RAGE axis may promote tumor cell proliferation, angiogenesis, and metastasis through NF-κB activation. | Role still under investigation; more evidence in gastrointestinal and breast cancers. |