Back to Journals » Drug Design, Development and Therapy » Volume 13

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


Checked for plagiarism Yes

Review by Single-blind

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

Creative Commons License This work is published and licensed by Dove Medical Press Limited. The full terms of this license are available at and incorporate the Creative Commons Attribution - Non Commercial (unported, v3.0) License. By accessing the work you hereby accept the Terms. Non-commercial uses of the work are permitted without any further permission from Dove Medical Press Limited, provided the work is properly attributed. For permission for commercial use of this work, please see paragraphs 4.2 and 5 of our Terms.

Download Article [PDF]  View Full Text [HTML][Machine readable]