莱比锡大学研究人员识别出GPR133受体作为骨骼健康的关键调控点1。该受体能够激活促进骨形成的成骨细胞，同时抑制导致骨丧失的破骨细胞活性1。研究团队由鲁道夫·申克海默生物化学研究所的Ines Liebscher教授主导1。
通过计算机辅助筛选，研究人员发现了实验性化合物AP503作为GPR133的刺激剂1。在动物实验中，AP503在健康小鼠和骨质疏松样骨丧失小鼠中均显著增强了骨强度1。早期研究还表明，该化合物激活GPR133同样能够增强骨骼肌力量1，这对老龄人群具有潜在临床应用价值。
德国约600万人患有骨质疏松症，其中大多数为女性1。相关研究已发表于《Signal Transduction and Targeted Therapy》1。
Researchers at Leipzig University have identified the GPR133 receptor as a critical molecular target for bone health, offering a promising new avenue for treating osteoporosis.1 The receptor works by activating bone-forming cells while simultaneously slowing bone loss, according to findings led by Professor Ines Liebscher at the Rudolf Schoenheimer Institute of Biochemistry.1 An experimental compound called AP503, discovered through computer-aided screening, significantly enhanced bone density in both healthy mice and those with osteoporosis-like bone loss.1 The compound also showed potential to strengthen skeletal muscle, suggesting broad therapeutic applications particularly for aging populations.1
The research demonstrates that activating GPR133 promotes osteoblast activity—the cells responsible for building bone—while reducing osteoclast activity, which drives bone degradation.1 In preclinical studies, AP503 strengthened bone in both normal and osteoporotic animal models.1 The findings are particularly relevant given that approximately 6 million people in Germany suffer from osteoporosis, with the majority being women.1 The team's work has been published in Signal Transduction and Targeted Therapy (DOI: 10.1038/s41392-025-02291-y).1
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