AGEs have a range of pathological effects, such as:
* Increased vascular permeability.
* Increased arterial stiffness
* Inhibition of vascular dilation by interfering with nitric oxide.
* Oxidizing LDL.
* Binding cells—including macrophage, endothelial, and mesangial—to induce the secretion of a variety of cytokines. 
* Enhanced oxidative stress.
* Hemoglobin-AGE levels are elevated in diabetic individuals and other AGE proteins have been shown in experimental models to accumulate with time, increasing from 5-50 fold over periods of 5–20 weeks in the retina, lens and renal cortex of diabetic rats. The inhibition of AGE formation reduced the extent of nephropathy in diabetic rats. Therefore, substances that inhibit AGE formation may limit the progression of disease and may offer new tools for therapeutic interventions in the therapy of AGE-mediated disease.
* AGEs have specific cellular receptors; the best-characterized are those called RAGE. The activation of cellular RAGE on endothelium, mononuclear phagocytes, and lymphocytes triggers the generation of free radicals and the expression of inflammatory gene mediators. Such increases in oxidative stress lead to the activation of the transcription factor NF-κB and promote the expression of NF-κB regulated genes that have been associated with atherosclerosis.