RAGE deficiency induces a proinflammatory phenotype in bones and osteoblasts through PPAR-a suppression

Aims: Diabetes mellitus is associated with bone loss, increased fracture rate and reduced bone healing. Accumulation of advanced glycation end products (AGE) and associated overexpression of the receptor for AGE (RAGE) have been implicated in the pathogenesis of bone disease in diabetes. Although the AGE-RAGE interaction is well known for the sustained induction of inflammatory process, the physiologic role of RAGE in bone tissue is not clear. Remarkably, RAGE deficiency induces a proinflammatory phenotype in bones and osteoblasts. Therefore, we aimed to study the mechanism of underlying inflammatory processes i…