Fig. 1Suggested mechanism of advanced glycation end-products (AGEs) in diabetic vascular complications. RAGE, receptor for advanced glycation end-product; NF-κB, nuclear factor κB; RAS, renin-angiotensin system; TZD, thiazolidinediones; GLP-1, glucagon like peptide-1; DPP-4, dipeptidylpeptide-4; sRAGE, soluble receptor for advanced glycation end-product; ROS, reactive oxygen species; eNOS, endothelial nitric oxide synthase; NADPH, nicotinamide adenine dinucleotide phosphate; IL, interleukin; TNF-α, tumor necrosis factor α.
Table 1Agents known to modulate AGEs
Agents |
Suggested effects |
References |
Pravastatin |
Reduce tubular damage in diabetic nephropathy in tubular cells and attenuate AGEs-induced apoptosis |
[41] |
Atorvastatin |
Inhibit AGE formation through its anti-oxidative activity |
[42] |
Telmisartan |
Inhibit the expression of oxidative stress and inflammatory markers by inhibiting signal transduction by AGEs and expression of arteriosclerosis-related genes |
[43,44] |
Ramipril |
Inhibit the expression of oxidative stress and inflammatory markers by inhibiting signal transduction by AGEs |
[45] |
Rosiglitazone |
Reduce the expression of RAGE on the myocardium and attenuate cardiac fibrosis and ventricular diastolic function |
[46] |
Exendin-4 |
Inhibit the AGE-RAGE mediated damage in tubular cells to attenuate the development and progression of diabetic nephropathy |
[47] |
Linagliptin |
Inhibit AGE-RAGE–evoked oxidative stress generation |
[48,49] |
Aminoguanidine |
Prevent cardiac hypertrophy and arterial stiffening in diabetic cardiomyopathy |
[50,51,52] |
ALT-711 |
AGE cross-link breaker |
[52] |
Alagebrium |
AGE cross-link breaker |
[45] |
sRAGE |
Competitive inhibitor of RAGE |
[32] |