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Updated: Nov 9, 2025

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GPR35 regulates osteogenesis via the Wnt/GSK3β/β-catenin signaling pathway

Yao Zhang1, Tingwang Shi1, Yaohua He1

  • 1Department of Orthopaedics, Shanghai Jiao Tong University Affiliated Sixth People's Hospital, Shanghai, China.

Biochemical and Biophysical Research Communications
|April 11, 2021
PubMed

Insights

Osteoporosis is linked to reduced G protein-coupled receptor 35 (GPR35) in stem cells. Activating GPR35 with zaprinast shows promise for treating bone loss in osteoporosis.

Area of Science:

  • Biomedical research
  • Cell biology
  • Bone biology

Background:

  • Osteoporosis is a growing concern with an aging population.
  • Bone marrow mesenchymal stem cells (BMSCs) are crucial for bone health.
  • G protein-coupled receptor 35 (GPR35) role in bone metabolism is under investigation.

Purpose of the Study:

  • To investigate the role of GPR35 in osteoporosis.
  • To explore GPR35's impact on BMSC function and bone mass.
  • To evaluate GPR35 agonists as a potential osteoporosis treatment.

Main Methods:

  • Assessed GPR35 expression in osteoporosis patients and mice.
  • Utilized GPR35 knockout and overexpression models in BMSCs.
  • Examined effects on BMSC proliferation, osteogenesis, and beta-catenin activity.
  • Administered GPR35 agonist zaprinast to ovariectomized mice.

Main Results:

  • GPR35 expression was suppressed in osteoporosis.
  • GPR35 enhanced BMSC osteogenic differentiation and proliferation.
  • GPR35 deficiency impaired bone mass and beta-catenin activity.
  • Zaprinast treatment reversed ovariectomy-induced bone loss.

Conclusions:

  • GPR35 plays a critical role in maintaining bone mass and BMSC function.
  • GPR35 is a potential therapeutic target for osteoporosis.
  • The GPR35 agonist zaprinast demonstrates therapeutic potential for osteoporosis treatment.
Keywords:
GPR35GSK3βOsteogenesisOsteoporosisβ-Catenin

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