• 文献检索
  • 文档翻译
  • 深度研究
  • 学术资讯
  • Suppr Zotero 插件Zotero 插件
  • 邀请有礼
  • 套餐&价格
  • 历史记录
应用&插件
Suppr Zotero 插件Zotero 插件浏览器插件Mac 客户端Windows 客户端微信小程序
定价
高级版会员购买积分包购买API积分包
服务
文献检索文档翻译深度研究API 文档MCP 服务
关于我们
关于 Suppr公司介绍联系我们用户协议隐私条款
关注我们

Suppr 超能文献

核心技术专利:CN118964589B侵权必究
粤ICP备2023148730 号-1Suppr @ 2026

文献检索

告别复杂PubMed语法,用中文像聊天一样搜索,搜遍4000万医学文献。AI智能推荐,让科研检索更轻松。

立即免费搜索

文件翻译

保留排版,准确专业,支持PDF/Word/PPT等文件格式,支持 12+语言互译。

免费翻译文档

深度研究

AI帮你快速写综述,25分钟生成高质量综述,智能提取关键信息,辅助科研写作。

立即免费体验

免疫骨质疏松症的病理生理学:创新的治疗靶点。

The pathophysiology of immunoporosis: innovative therapeutic targets.

机构信息

Orthopedics Research Laboratory, Research Center, Hôpital du Sacré-Cœur de Montréal, Université de Montréal, 5400 boul. Gouin ouest, Montréal, Québec, H4J 1C5, Canada.

出版信息

Inflamm Res. 2021 Aug;70(8):859-875. doi: 10.1007/s00011-021-01484-9. Epub 2021 Jul 16.

DOI:10.1007/s00011-021-01484-9
PMID:34272579
Abstract

BACKGROUND

The physiological balance between bone resorption and bone formation is now known to be mediated by a cascade of events parallel to the classic osteoblast-osteoclast interaction. Thus, osteoimmunology now encompasses the role played by other cell types, such as cytokines, lymphocytes and chemokines, in immunological responses and how they help modulate bone metabolism. All these factors have an impact on the RANK/RANKL/OPG pathway, which is the major pathway for the maturation and resorption activity of osteoclast precursor cells, responsible for osteoporosis development. Recently, immunoporosis has emerged as a new research area in osteoimmunology dedicated to the immune system's role in osteoporosis.

METHODS

The first part of this review presents theoretical concepts on the factors involved in the skeletal system and osteoimmunology. Secondly, existing treatments and novel therapeutic approaches to treat osteoporosis are summarized. These were selected from to the most recent studies published on PubMed containing the term osteoporosis. All data relate to the results of in vitro and in vivo studies on the osteoimmunological system of humans, mice and rats.

FINDINGS

Treatments for osteoporosis can be classified into two categories. They either target osteoclastogenesis inhibition (denosumab, bisphosphonates), or they aim to restore the number and function of osteoblasts (romozumab, abaloparatide). Even novel therapies, such as resolvins, gene therapy, and mesenchymal stem cell transplantation, fall within this classification system.

CONCLUSION

This review presents alternative pathways in the pathophysiology of osteoporosis, along with some recent therapeutic breakthroughs to restore bone homeostasis.

摘要

背景

现在已知,骨吸收和骨形成之间的生理平衡是由一系列与经典成骨细胞-破骨细胞相互作用平行的事件级联介导的。因此,骨免疫学现在包括其他细胞类型(如细胞因子、淋巴细胞和趋化因子)在免疫反应中的作用,以及它们如何帮助调节骨代谢。所有这些因素都对 RANK/RANKL/OPG 途径有影响,该途径是破骨细胞前体细胞成熟和吸收活性的主要途径,负责骨质疏松症的发展。最近,免疫骨质疏松症作为骨免疫学中的一个新的研究领域出现,致力于研究免疫系统在骨质疏松症中的作用。

方法

本综述的第一部分介绍了骨骼系统和骨免疫学中涉及的因素的理论概念。其次,总结了现有的骨质疏松症治疗方法和新的治疗方法。这些方法是从 Pubmed 上发表的关于骨质疏松症的最新研究中选择的,所有数据均涉及人类、小鼠和大鼠骨免疫学系统的体外和体内研究结果。

发现

骨质疏松症的治疗方法可分为两类。一类是抑制破骨细胞生成(地舒单抗、双磷酸盐),另一类是恢复成骨细胞的数量和功能(罗莫珠单抗、abaloparatide)。即使是新型疗法,如 resolvins、基因治疗和间充质干细胞移植,也属于这一分类系统。

结论

本综述介绍了骨质疏松症病理生理学中的替代途径,以及一些恢复骨稳态的最新治疗突破。

相似文献

1
The pathophysiology of immunoporosis: innovative therapeutic targets.免疫骨质疏松症的病理生理学:创新的治疗靶点。
Inflamm Res. 2021 Aug;70(8):859-875. doi: 10.1007/s00011-021-01484-9. Epub 2021 Jul 16.
2
Osteocyte-Related Cytokines Regulate Osteoclast Formation and Bone Resorption.骨细胞相关细胞因子调节破骨细胞的形成和骨吸收。
Int J Mol Sci. 2020 Jul 21;21(14):5169. doi: 10.3390/ijms21145169.
3
Osteoporosis Due to Hormone Imbalance: An Overview of the Effects of Estrogen Deficiency and Glucocorticoid Overuse on Bone Turnover.激素失衡导致的骨质疏松症:雌激素缺乏和糖皮质激素过度使用对骨代谢的影响概述。
Int J Mol Sci. 2022 Jan 25;23(3):1376. doi: 10.3390/ijms23031376.
4
Aging increases stromal/osteoblastic cell-induced osteoclastogenesis and alters the osteoclast precursor pool in the mouse.衰老会增加基质/成骨细胞诱导的破骨细胞生成,并改变小鼠体内破骨细胞前体细胞库。
J Bone Miner Res. 2005 Sep;20(9):1659-68. doi: 10.1359/JBMR.050503. Epub 2005 May 2.
5
Interleukin-20 differentially regulates bone mesenchymal stem cell activities in RANKL-induced osteoclastogenesis through the OPG/RANKL/RANK axis and the NF-κB, MAPK and AKT signalling pathways.白细胞介素-20 通过 OPG/RANKL/RANK 轴和 NF-κB、MAPK 和 AKT 信号通路,差异调节 RANKL 诱导的破骨细胞发生过程中的骨间充质干细胞活性。
Scand J Immunol. 2020 May;91(5):e12874. doi: 10.1111/sji.12874. Epub 2020 Mar 10.
6
Local Production of Osteoprotegerin by Osteoblasts Suppresses Bone Resorption.成骨细胞产生的护骨素抑制骨吸收。
Cell Rep. 2020 Sep 8;32(10):108052. doi: 10.1016/j.celrep.2020.108052.
7
The cross-talk between osteoclasts and osteoblasts in response to strontium treatment: involvement of osteoprotegerin.成骨细胞与破骨细胞间的串扰在锶治疗中的反应:骨保护素的参与。
Bone. 2011 Dec;49(6):1290-8. doi: 10.1016/j.bone.2011.08.031. Epub 2011 Sep 9.
8
[The OPG/RANKL/RANK system and bone resorptive disease].[骨保护素/核因子κB受体活化因子配体/核因子κB受体活化因子系统与骨吸收性疾病]
Sheng Wu Gong Cheng Xue Bao. 2003 Nov;19(6):655-60.
9
IDH2 deficiency increases bone mass with reduced osteoclastogenesis by limiting RANKL expression in osteoblasts.IDH2 缺陷通过限制成骨细胞中 RANKL 的表达来增加骨量并减少破骨细胞生成。
Bone. 2019 Dec;129:115056. doi: 10.1016/j.bone.2019.115056. Epub 2019 Aug 31.
10
Osteoclast differentiation by RANKL and OPG signaling pathways.破骨细胞通过 RANKL 和 OPG 信号通路的分化。
J Bone Miner Metab. 2021 Jan;39(1):19-26. doi: 10.1007/s00774-020-01162-6. Epub 2020 Oct 20.

引用本文的文献

1
Causal Associations of the Alterations in Peripheral Blood Immune Cell Characteristics on the Incidence of Osteoporosis: A Bidirectional Mendelian Randomization Study.外周血免疫细胞特征改变与骨质疏松症发病率的因果关联:一项双向孟德尔随机化研究
Ther Clin Risk Manag. 2025 Aug 14;21:1259-1275. doi: 10.2147/TCRM.S518164. eCollection 2025.
2
Ganoderic Acid A Prevented Osteoporosis by Modulating the PIK3CA/p-Akt/TWIST1 Signaling Pathway.灵芝酸A通过调节PIK3CA/p-Akt/TWIST1信号通路预防骨质疏松症。
Food Sci Nutr. 2025 Apr 14;13(4):e70177. doi: 10.1002/fsn3.70177. eCollection 2025 Apr.
3
The CD163/TWEAK/Fn14 axis: A potential therapeutic target for alleviating inflammatory bone loss.

本文引用的文献

1
The Mediterranean Diet in Osteoporosis Prevention: An Insight in a Peri- and Post-Menopausal Population.地中海饮食在骨质疏松预防中的作用:绝经前后人群的新视角。
Nutrients. 2021 Feb 6;13(2):531. doi: 10.3390/nu13020531.
2
Betulinic Acid Protects From Bone Loss in Ovariectomized Mice and Suppresses RANKL-Associated Osteoclastogenesis by Inhibiting the MAPK and NFATc1 Pathways.桦木酸可保护去卵巢小鼠免受骨质流失,并通过抑制丝裂原活化蛋白激酶(MAPK)和活化T细胞核因子c1(NFATc1)信号通路来抑制与核因子κB受体活化因子配体(RANKL)相关的破骨细胞生成。
Front Pharmacol. 2020 Jul 7;11:1025. doi: 10.3389/fphar.2020.01025. eCollection 2020.
3
Inhibitory effect of oolonghomobisflavan B on osteoclastogenesis by suppressing p38 MAPK activation.
CD163/TWEAK/Fn14轴:减轻炎症性骨质流失的潜在治疗靶点。
J Orthop Translat. 2024 Oct 4;49:82-95. doi: 10.1016/j.jot.2024.09.002. eCollection 2024 Nov.
4
An exploration of the causal relationship between 731 immunophenotypes and osteoporosis: a bidirectional Mendelian randomized study.731种免疫表型与骨质疏松症之间因果关系的探索:一项双向孟德尔随机研究。
Front Endocrinol (Lausanne). 2024 Jul 17;15:1341002. doi: 10.3389/fendo.2024.1341002. eCollection 2024.
5
Denosumab vs. bisphosphonates in primary osteoporosis: a meta-analysis of comparative safety in randomized controlled trials.地舒单抗与双膦酸盐类药物治疗原发性骨质疏松症的比较:随机对照试验中安全性的荟萃分析。
Osteoporos Int. 2024 Aug;35(8):1377-1393. doi: 10.1007/s00198-024-07118-0. Epub 2024 May 11.
6
Deubiquitinase USP17 Regulates Osteoblast Differentiation by Increasing Osterix Protein Stability.去泛素化酶 USP17 通过增加骨形态发生蛋白 2 蛋白稳定性调节成骨细胞分化。
Int J Mol Sci. 2023 Oct 17;24(20):15257. doi: 10.3390/ijms242015257.
7
Understanding the Consequences of Fatty Bone and Fatty Muscle: How the Osteosarcopenic Adiposity Phenotype Uncovers the Deterioration of Body Composition.了解脂肪骨和脂肪肌肉的后果:骨肌减少性肥胖表型如何揭示身体成分的恶化。
Metabolites. 2023 Oct 7;13(10):1056. doi: 10.3390/metabo13101056.
8
MiR-224-5p inhibits osteoblast differentiation and impairs bone formation by targeting Runx2 and Sp7.微小RNA-224-5p通过靶向Runx2和Sp7抑制成骨细胞分化并损害骨形成。
Cytotechnology. 2023 Dec;75(6):505-516. doi: 10.1007/s10616-023-00593-z. Epub 2023 Sep 5.
9
Inhibition of Toll-Like Receptor 4 Signaling Pathway Accelerates the Repair of Avascular Necrosis of Femoral Epiphysis through Regulating Macrophage Polarization in Perthes Disease.抑制 Toll 样受体 4 信号通路通过调节佩特兹病中的巨噬细胞极化加速股骨头骨骺缺血性坏死的修复。
Tissue Eng Regen Med. 2023 Jun;20(3):489-501. doi: 10.1007/s13770-023-00529-w. Epub 2023 Apr 11.
10
Estradiol and zinc-doped nano hydroxyapatite as therapeutic agents in the prevention of osteoporosis; oxidative stress status, inflammation, bone turnover, bone mineral density, and histological alterations in ovariectomized rats.雌二醇和锌掺杂纳米羟基磷灰石作为预防骨质疏松症的治疗剂;去卵巢大鼠的氧化应激状态、炎症、骨转换、骨矿物质密度及组织学改变
Front Physiol. 2022 Sep 19;13:989487. doi: 10.3389/fphys.2022.989487. eCollection 2022.
乌龙茶二氢黄酮 B 通过抑制 p38MAPK 激活抑制破骨细胞生成。
Bioorg Med Chem Lett. 2020 Sep 15;30(18):127429. doi: 10.1016/j.bmcl.2020.127429. Epub 2020 Jul 21.
4
The Mediterranean diet and menopausal health: An EMAS position statement.《地中海饮食与绝经健康:欧洲绝经学会立场声明》。
Maturitas. 2020 Sep;139:90-97. doi: 10.1016/j.maturitas.2020.07.001. Epub 2020 Jul 15.
5
Betulinic Acid Inhibits RANKL-Induced Osteoclastogenesis via Attenuating Akt, NF-κB, and PLCγ2-Ca Signaling and Prevents Inflammatory Bone Loss.桦木酸通过抑制 Akt、NF-κB 和 PLCγ2-Ca 信号通路抑制 RANKL 诱导的破骨细胞生成,防止炎症性骨丢失。
J Nat Prod. 2020 Apr 24;83(4):1174-1182. doi: 10.1021/acs.jnatprod.9b01212. Epub 2020 Apr 2.
6
[Pain management in osteoporosis].[骨质疏松症的疼痛管理]
Schmerz. 2020 Feb;34(1):91-104. doi: 10.1007/s00482-020-00445-1.
7
Cost-effectiveness of denosumab for high-risk postmenopausal women with osteoporosis in Thailand.地舒单抗治疗泰国绝经后骨质疏松症高危女性的成本效果分析。
J Med Econ. 2020 Jul;23(7):776-785. doi: 10.1080/13696998.2020.1730381. Epub 2020 Feb 28.
8
Abaloparatide exhibits greater osteoanabolic response and higher cAMP stimulation and β-arrestin recruitment than teriparatide.与特立帕肽相比,阿巴洛帕替德表现出更强的骨合成代谢反应、更高的环磷酸腺苷(cAMP)刺激作用和β-抑制蛋白募集作用。
Physiol Rep. 2019 Oct;7(19):e14225. doi: 10.14814/phy2.14225.
9
New Frontiers in Osteoporosis Therapy.骨质疏松症治疗的新前沿。
Annu Rev Med. 2020 Jan 27;71:277-288. doi: 10.1146/annurev-med-052218-020620. Epub 2019 Sep 11.
10
The efficacy of sustained-release chitosan microspheres containing recombinant human parathyroid hormone on MRONJ.含重组人甲状旁腺激素的壳聚糖缓释微球对下颌骨放射性骨坏死的疗效
Braz Oral Res. 2019 Aug 29;33:e086. doi: 10.1590/1807-3107bor-2019.vol33.0086.