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细胞因子在绝经后骨质疏松症发病机制中的作用
引用本文:邹世恩,张绍芬.细胞因子在绝经后骨质疏松症发病机制中的作用[J].中国骨质疏松杂志,2012,18(4):375-380.
作者姓名:邹世恩  张绍芬
作者单位:复旦大学附属妇产科医院妇科, 上海,200011
摘    要:雌激素、免疫细胞因子及骨代谢三者相互作用,绝经后骨质疏松症主要与雌激素缺乏导致细胞因子激活破骨细胞的活性密切相关。雌激素缺乏导致巨噬细胞和T细胞分泌IL-1和TNFα,抑制调节性T细胞增殖和成熟,促进NFκB、IL-15和IL-17的产生,从而诱导破骨细胞发展;抑制成骨细胞和骨系细胞产生OPG,促进RANK-RANKL相互作用,导致破骨细胞活性增强;抑制成骨细胞和骨细胞的TGFβ,减少破骨细胞凋亡。

关 键 词:绝经后骨质疏松症  雌激素  细胞因子

The role of cytokines in the pathogenesis of postmenopausal osteoporosis
ZOU Shien , ZHANG Shaofen.The role of cytokines in the pathogenesis of postmenopausal osteoporosis[J].Chinese Journal of Osteoporosis,2012,18(4):375-380.
Authors:ZOU Shien  ZHANG Shaofen
Institution:.Department of Gynecology,The Obstetritcs and Gynecology Hospital of Fudan University,Shanghai 200011,China
Abstract:Estrogen,cytokines,and,bone metabolism are closely related.Postmenopausal osteoporosis is mainly due to estrogen deficiency leading to cytokine-mediated activation of osteoclasts.Lack of estrogen causes the secretion of IL-1 and TNFα of macrophages and T cells,the inhibition of proliferation and maturation of regulatory T cells,promoting the production of NFκB,IL-15,and IL-17,and then resulting in osteoclast development.Lack of estrogen can also inhibit the production of OPG,promote the interaction of RANK and RANKL,leading to increase of osteoclast activity.Lack of estrogen can also inhibit the production of TGFβ to reduce osteoclast apoptosis.
Keywords:Postmenopausal osteoporosis  Estrogen  Cytokine
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