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| cAMP-PKA/EPAC信号转导与骨质疏松症的作用机制研究进展 |
| Research progress on the mechanism of cAMP-PKA/EPAC signal transduction and osteoporosis |
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| DOI：10.3969/j.issn.1006-7108.2025.06.014 |
| 中文关键词: cAMP-PKA/EPAC信号转导 骨髓间充质干细胞 成骨细胞 破骨细胞 |
| 英文关键词:cAMP-PKA/EPAC signal transduction Bone marrow mesenchymal stem cells Osteoblast Osteoclast |
| 基金项目:甘肃省联合科研基金项目（24JRRA878）；2025年省级人才项目重点一般项目（2025RCXM006）；甘肃省自然科学基金项目（24JRRA1020）；甘肃省科技计划项目重点研发计划国际科技合作类（25YFWA024） |
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| 中文摘要: |
| 骨质疏松症与低骨密度有关，低骨密度与高发病率、死亡率和社会经济负担密切相关。cAMP是该信号通路的初始活化剂，通过激活cAMP依赖性蛋白激酶（PKA）和cAMP激活的交换蛋白（EPAC）来介导其生物学效应。值得注意，cAMP的增加促进骨形成，并减缓骨质疏松的发生。然而，高水平的cAMP导致骨髓间充质干细胞的过度增殖和分化，加速骨吸收，加剧骨质疏松的发展。cAMP对骨质疏松症的影响具有双重性，取决于其在骨细胞中的浓度和调节机制。因此，本文综述了cAMP-PKA/EPAC 信号在骨质疏松症生物学中的理解，并讨论了其在骨髓间充质干细胞、成骨细胞和破骨细胞环境的作用基础。 |
| 英文摘要: |
| Osteoporosis, characterized by low bone mineral density, imposes significant morbidity, mortality, and socioeconomic burden. The cAMP signaling pathway serves as the pivotal initiator in this context, orchestrating its effects through the activation of cAMP-dependent protein kinase (PKA) and CAMP-activated exchange protein (EPAC). Notably, heightened levels of cAMP foster bone formation and mitigate the onset of osteoporosis. Conversely, excessive cAMP levels prompt the over-proliferation and differentiation of bone marrow mesenchymal stem cells, hastening bone resorption and exacerbating osteoporosis progression. The impact of cAMP on osteoporosis manifests a dualistic nature contingent upon its concentration within bone cells and the intricacies of its regulatory mechanisms. Hence, this review comprehensively examines the implications of the cAMP-PKA/EPAC signaling pathway in osteoporosis biology, shedding light on its nuanced role across bone marrow mesenchymal stem cells, osteoblasts and the osteoclasts microenvironment. |
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