PPARγ in bone homeostasis

Yihong Wan

Research output: Contribution to journalReview articlepeer-review

107 Scopus citations


The nuclear receptor peroxisome proliferator-activated receptor (PPAR)γ is a crucial cellular and metabolic switch that regulates many physiologic and disease processes. Emerging evidence reveals that PPARγ is also a key modulator of skeletal remodeling. Long-term use of rosiglitazone, a synthetic PPARγ agonist and a drug to treat insulin resistance, increases fracture rates among patients with diabetes. Recent studies have revealed that PPARγ activation not only suppresses osteoblastogenesis, but also activates osteoclastogenesis, thereby decreasing bone formation while sustaining or increasing bone resorption. The pro-osteoclastogenic effect of rosiglitazone is mediated by a transcriptional network comprised of PPARγ, PPAR-gamma coactivator 1β and estrogen-related receptor α, which promotes both osteoclast differentiation and mitochondrial activation. Therefore, PPARγ plays dual roles in bone homeostasis by regulating both mesenchymal and hematopoietic lineages.

Original languageEnglish (US)
Pages (from-to)722-728
Number of pages7
JournalTrends in Endocrinology and Metabolism
Issue number12
StatePublished - Dec 2010

ASJC Scopus subject areas

  • Endocrinology, Diabetes and Metabolism
  • Endocrinology


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