|本期目录/Table of Contents|

[1]李立军 综述,倪东馗 审校.雌激素缺乏在PMO发病中的作用机制研究进展[J].天津医科大学学报,2022,28(05):560.
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雌激素缺乏在PMO发病中的作用机制研究进展(PDF)
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《天津医科大学学报》[ISSN:1006-8147/CN:12-1259/R]

卷:
28卷
期数:
2022年05期
页码:
560
栏目:
综述
出版日期:
2022-09-20

文章信息/Info

Title:
-
文章编号:
1006-8147(2022)05-0560-04
作者:
李立军 综述倪东馗 审校
(天津医科大学第二医院骨科,天津300211)
Author(s):
-
关键词:
绝经后骨质疏松症雌激素受体氧化应激免疫反应
Keywords:
-
分类号:
R363
DOI:
-
文献标志码:
A
摘要:
绝经后骨质疏松症(PMO)是由于女性雌激素缺乏骨重塑失衡引起的骨量减少、骨折风险增加的一种骨骼疾病。大量研究已证实,雌激素缺乏在PMO的发生、发展中发挥主要作用。雌激素缺乏通过雌激素受体的介导,调控下游通路以及破骨与成骨;雌激素作为抗氧化剂,调控骨微环境中氧化应激状态以及骨重塑;雌激素缺乏还能通过调控T细胞和B细胞的激活诱发免疫反应,调控骨重塑。以上雌激素缺乏引起的多重机制联合作用在骨重塑中发挥重要的调控作用。通过对绝经后骨质疏松症多种发病机制的研究,可进一步加深临床医生对PMO的认知,并为寻找新的治疗方法提供思路。
Abstract:
-

参考文献/References:

[1] 中华医学会骨质疏松和骨矿盐疾病分会.原发性骨质疏松症诊疗指南(2017)[J].中国骨质疏松杂志,2019,25(3):281-309.
[2] DOMAZETOVIC V,MARCUCCI G,IANTOMASI T,et al.Oxidative stress in bone remodeling: role of antioxidants[J].Clin Cases Miner Bone Metab,2017,14(2):209-216.
[3] D′AMELIO P.The immune system and postmenopausal osteoporosis[J].Immunol Invest,2013,42(7):544-554.
[4] KHALID A B,KRUM S A. Estrogen receptors alpha and beta in bone [J].Bone,2016,87:130-135.
[5] MOHAMAD N V,IMA-NIRWANA S,CHIN K Y. Are oxidative stress and inflammation mediators of bone loss due to estrogen deficiency?A review of current evidence [J].Endocr Metab Immune Disord Drug Targets,2020,20(9):1478-1487.
[6] STREICHER C,HEYNY A,ANDRUKHOVA O,et al.Estrogen regulates bone turnover by targeting rankl expression in bone lining cells[J].Sci Rep,2017,7(1):6460.
[7] GUTTERIDGE J M C,HALLIWELL B. Mini-review:oxidative stress,redox stress or redox success?[J].Biochem Biophys Res Commun,2018,502(2):183-186.
[8] DOMAZETOVIC V,MARCUCCI G,IANTOMASI T,et al. Oxidative stress in bone remodeling:role of antioxidants[J].Clin Cases Miner Bone Metab,2017,14(2):209-216.
[9] SCHRDER K. NADPH oxidases in bone homeostasis and osteoporosis[J].Free Radic Biol Med,2019,132:67-72.
[10] SHIN H J,PARK H,SHIN N,et al. p66shc siRNA Nanoparticles ameliorate chondrocytic mitochondrial dysfunction in osteoarthritis[J].Int J Nanomedicine,2020,15:2379-2390.
[11] MONIQUE O,LILIAN C S,MARIA M N,et al. A long-term estrogen deficiency in ovariectomized mice is associated with disturbances in fatty acid oxidation and oxidative stress [J].Rev Bras Ginecol Obstet,2018,40(5):251-259.
[12] WANG C,XIAO F,QU X,et al.Sitagliptin,an anti-diabetic drug,suppresses estrogen deficiency-induced osteoporosis in vivo and inhibits rankl-induced osteoclast formation and bone resorption in vitro[J].Front Pharmacol,2017,8:407.
[13] CALLAWAY D A,JIANG J X.Reactive oxygen species and oxidative stress in osteoclastogenesis,skeletal aging and bone diseases[J]. J Bone Miner Metab,2015,33(4):359-370.
[14] CRONIN B E,ALLSOPP P J,SLEVIN M M,et al.The effect of weight change over a 2-year period on inflammatory status in postmenopausal women[J].Eur J Clin Nutr,2018,72(3):388-393.
[15] ZHANG J,WANG H,YANG S,et al.Comparison of lipid profiles and inflammation in pre- and post-menopausal women with cerebral infarction and the role of atorvastatin in such populations[J].Lipids Health Dis,2018,17(1):20.
[16] UEHARA I A,SOLDI L R,SILVA M.Current perspectives of osteoclastogenesis through estrogen modulated immune cell cytokines[J].Life Sci,2020,256:117921.
[17] PIETSCHMANN P,MECHTCHERIAKOVA D,MESHCHERYAKOVA A,et al. Immunology of osteoporosis:a mini-review[J].Gerontology,2016,62(2):128-137.
[18] D′AMELIO P,GRIMALDI A,BELLA S D,et al.Estrogen deficiency increases osteoclastogenesis up-regulating T cells activity:a key mechanism in osteoporosis [J].Bone,2008,43(1):92-100.
[19] WALSH M C, CHOI Y. Biology of the RANKL-RANK-OPG system in immunity,bone,and beyond[J].Front Immunol,2014,5:511.
[20] RYAN M R, SHEPHERD R, LEAVEY J K,et al. An IL-7-dependent rebound in thymic T cell output contributes to the bone loss induced by estrogen deficiency[J].Proc Natl Acad Sci U S A,2005,102(46):16735-16740.
[21] ZHAO B.TNF and bone remodeling[J].Curr Osteoporos Rep,2017,15(3):126-134.
[22] WEITZMANN M N.Bone and the immune system[J].Toxicol Pathol,2017,45(7):911-924.
[23] TAKAYANAGI H, OGASAWARA K, HIDA S,et al.T-cell-mediated regulation of osteoclastogenesis by signalling cross-talk between RANKL and IFN-gamma[J].Nature,2000,408(6812):600-605.
[24] PONZETTI M, RUCCI N.Updates on osteoimmunology:what′s new on the cross-talk between bone and immune system[J].Front Endocrinol(Lausanne),2019,10:236.
[25] KIM J H, SIM J H,LEE S,et al.Interleukin-7 induces osteoclast formation via STAT5,independent of receptor activator of NF-kappaB ligand[J].Front Immunol,2017,8:1376.
[26] XIAO L, XIAO Y.The autophagy in osteoimmonology: self-eating,maintenance,and beyond[J].Front Endocrinol(Lausanne),2019,10:490.
[27] LI C, LI G, LIU M,et al.Paracrine effect of inflammatory cytokine-activated bone marrow mesenchymal stem cells and its role in osteoblast function[J]. J Biosci Bioeng,2016,121(2):213-219.
[28] HORWOOD N J.Macrophage polarization and bone formation: a review [J].Clin Rev Allergy Immunol,2016,51(1):79-86.
[29] SCHLUNDT C, KHASSAWNA T E, SERRA A,et al. Macrophages in bone fracture healing: their essential role in endochondral ossification[J].Bone,2018,106:78-89.
[30] ADAMOPOULOS I E.Inflammation in bone physiology and pathology[J].Curr Opin Rheumatol,2018,30(1):59-64.

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备注/Memo

备注/Memo:
基金项目 国家自然科学基金(81702110);天津市科技计划项目(19KPXMRC00020)
作者简介 李立军(1977-),男,副主任医师,硕士,研究方向:骨质疏松,骨质疏松脆性骨折,关节、脊柱疾病;E-mail:lilijun6208@qq.com。
更新日期/Last Update: 2022-09-20