Bone metabolism is a complex physiological process that primarily involves osteoblast-mediated bone formation and osteoclast-mediated bone resorption, both of which are regulated by a variety of biological factors. There is increasing evidence that peroxisome proliferator-activated receptor γ (PPARγ) is a member of the nuclear receptor superfamily and plays an important role in lipid metabolism and bone metabolism. Through the PPARγ-dependent pathway, 15-deoxy-Δ12,14-prostaglandin J2 (15d-PGJ2) promotes the formation of marrow adipocytes and inhibits the formation of osteoblasts, resulting in bone loss and increasing the risk of fracture and osteoporosis. Recent studies have found that through the PPARγ-independent pathway, 15d-PGJ2 plays a regulatory role in bone metastasis of breast cancer, which can inhibit osteoclastogenesis and reduce bone destruction. The purpose of our review is to summarize the recent progress in elucidating the mechanisms and effects of 15d-PGJ2 in bone metabolism, which can serve as a novel therapeutic target for bone tumors, osteoporosis, rheumatoid arthritis (RA), and other bone diseases.
Keywords: adipogenesis; bone metabolism; bone metastasis; osteoblast; osteoporosis; rheumatoid arthritis.