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15-Deoxy-Δ12,14-prostaglandin J2 as a potential regulator of bone metabolism via PPARγ-dependent and independent pathways: a review

Authors Xiong Z, Luo P, Zhou J, Tan M

Received 25 February 2019

Accepted for publication 10 May 2019

Published 30 May 2019 Volume 2019:13 Pages 1879—1888

DOI https://doi.org/10.2147/DDDT.S206695

Checked for plagiarism Yes

Review by Single-blind

Peer reviewers approved by Ms Justinn Cochran

Peer reviewer comments 2

Editor who approved publication: Professor Manfred Ogris


Zhencheng Xiong,1,2 Pan Luo,1 Jun Zhou,2,3 Mingsheng Tan1–3

1Graduate School of Peking Union Medical College, Chinese Academy of Medical Sciences, Beijing, People’s Republic of China; 2Department of Spine Surgery, China-Japan Friendship Hospital, Beijing, People’s Republic of China; 3School of Clinical Medicine, Graduate School of Beijing University of Chinese Medicine, Beijing, People’s Republic of China

Abstract: 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: bone metabolism, osteoblast, adipogenesis, osteoporosis, rheumatoid arthritis, bone metastasis

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