In diabetic patients, advanced glycation end products (AGEs) accumulate in the vessels, kidney, skin, bones, and other tissues and results in diabetic vascular complications such as retinopathy, nephropathy, and neuropathy. Moreover, osteoporosis is caused by the deposition of AGEs in bone tissue. AGEs are cytotoxic to human gingival fibroblasts depending on their concentration and incubation time. AGEs increase inflammatory mediators such as monocyte chemotactic protein 1, interleukin 6, and vascular cell adhesion molecule 1in vascular adventitial fibroblasts. AGEs increase tumor necrosis factor-and induce cell apoptosis by activating the nuclear factor-? B pathway in human embryonic kidney and human mesangial cells. In addition, AGEs induce fibroblast apoptosis through the activation of reactive oxygen species, mitogen-activating protein kinase, and forkhead box protein O1 transcription factor. AGEs alter the biomechanical properties of tendon tissue. Cross-linked AGEs increase the stiffness of myocardial and vascular tissues.
Last date updated on July, 2014