This accelerates cell senescence, which leads to increased pro-inflammatory and pro-oxidant signaling by the senescence associated secretory phenotype (SASP) response, and induction of mitochondrial dysfunction, thereby propagating DNA damage and senescence to bystander cells.
Cardiovascular disease and renal disease for example are
accelerated in patients with diabetes and AGEs have been shown to induce
senescence in
cell types related to these diseases, such as endothelial progenitor
cells, vascular endothelial
cells and renal
cells.