切换至 "中华医学电子期刊资源库"

中华损伤与修复杂志(电子版) ›› 2023, Vol. 18 ›› Issue (06) : 538 -541. doi: 10.3877/cma.j.issn.1673-9450.2023.06.016

综述

巨噬细胞极化在骨质疏松中调控作用及机制的研究进展
陆宜仙, 张震涛, 夏德萌(), 王家林()   
  1. 200082 上海,海军军医大学基础医学院
    200120 上海市第七人民医院药学部
    200082 上海,海军军医大学第一附属医院特需诊疗科
  • 收稿日期:2023-05-15 出版日期:2023-12-01
  • 通信作者: 夏德萌, 王家林
  • 基金资助:
    上海市青年科技"启明星"A类计划(18QA1405400); 海南自然科学基金青年基金项目(823QN254)

Research progress of the regulating role and mechanism of macrophage polarization in osteoporosis

Yixian Lu, Zhentao Zhang, Demeng Xia(), Jialin Wang()   

  1. School of Basic Medical Sciences, Naval Military Medical University, Shanghai 200082, China
    Department of Pharmacy, Shanghai Seventh People′s Hospital, Shanghai 200120, China
    Department of Specialty Care, the First Affiliated Hospital of Shanghai Naval Medical University, Shanghai 200082, China
  • Received:2023-05-15 Published:2023-12-01
  • Corresponding author: Demeng Xia, Jialin Wang
引用本文:

陆宜仙, 张震涛, 夏德萌, 王家林. 巨噬细胞极化在骨质疏松中调控作用及机制的研究进展[J/OL]. 中华损伤与修复杂志(电子版), 2023, 18(06): 538-541.

Yixian Lu, Zhentao Zhang, Demeng Xia, Jialin Wang. Research progress of the regulating role and mechanism of macrophage polarization in osteoporosis[J/OL]. Chinese Journal of Injury Repair and Wound Healing(Electronic Edition), 2023, 18(06): 538-541.

骨质疏松症一直是备受关注的重点疾病之一。研究提示,巨噬细胞极化可能是影响骨质疏松症的重要机制之一。巨噬细胞极化过程中产生的细胞因子和激活的相关信号通路,与骨细胞、成骨细胞和破骨细胞等各种骨相关细胞相互作用,参与骨质疏松症的形成和转归。本文对巨噬细胞极化、表型转换的过程和调控机制,及其在骨愈合过程中的重要作用做综述,论述其治疗骨质疏松症的前景,为骨质疏松症靶点的选择提供新的思路。

Osteoporosis has been one of the major diseases that people pay attention to. Macrophage polarization may be one of the important mechanisms affecting osteoporosis. The cytokines produced during the process of macrophage polarization and the related signaling pathways activated interact with various bone-related cells such as osteocytes, osteoblasts and osteoclasts, and participate in the formation and outcome of osteoporosis. This paper mainly describes the generation and regulation mechanism of macrophage polarization and phenotypic transformation, summarizes its important role in the process of bone healing, discusses its prospects for the treatment of osteoporosis, and provides new ideas for the selection of osteoporosis targets.

[1]
Shane E, Burr D, Abrahamsen B, et al. Atypical subtrochanteric and diaphyseal femoral fractures: second report of a task force of the American society for bone mineral research[J]. J Bone Miner Res, 2014, 29(1): 1-23.
[2]
Khosla S, Burr D, Cauley J, et al. Bisphosphonate-associated osteonecrosis of the jaw: report of a task force of the American society for bone and mineral research[J]. J Bone Miner Res, 2007, 22(10): 1479-1491.
[3]
Li Y, Toraldo G, Li A, et al. B cells and T cells are critical for the preservation of bone homeostasis and attainment of peak bone mass in vivo[J]. Blood, 2007, 109(9) : 3839-3848.
[4]
Zaiss MM, Axmann R, Zwerina J, et al. Treg cells suppress osteoclast formation: a new link between the immune system and bone[J]. Arthritis and Rheumatism, 2007, 56(12):4104- 4112.
[5]
Godwin JW, Pinto AR, Rosenthal NA. Macrophages are required for adult salamander limb regeneration[J]. Proc Natl Acad Sci U S A, 2013, 110 (23) : 9415-9420.
[6]
Hayday AC. T cells and the lymphoid stress-surveillance response[J]. Immunity, 2009, 31(2): 184-196.
[7]
Strid J, Roberts SJ , Filler RB, et al. Acute upregulation of an NKG2D ligand promotes rapid reorganization of a local immune compartment with pleiotropic effects on carcinogenesis[J]. Nature Immunology, 2008, 9(2): 146-154.
[8]
Schmidt-Bleek K, Schell H , Kolar P, er al. Cellular composition of the initial fracture hematoma compared to a muscle hematoma: a study in sheep[J]. J Orthop Res, 2009, 27 (9) : 1147-1151.
[9]
Lienau J, Schmidt-Bleek K, Peters A, et al. Differential regulation of blood vessel formation between standard and delayed bone healing[J]. J Orthop Res, 2009, 27 (9): 1133-1140.
[10]
Biswas SK, Mantovani A. Macrophage plasticity and interaction with lymphocyte subsets: cancer as a paradigm[J]. Nat Immunol, 2010, 11(10): 889-896.
[11]
Sica A, Bronte V. Altered macrophage differentiation and immune dysfunction in tumor development[J]. J Clin Invest, 2007, 117(5): 1155-1166.
[12]
Mantovani A, Sozzani S, Locati M, et al. Macrophage polarization: tumor-associated macrophages as a paradigm for polarized M2 mononuclear phagocytes[J]. Trends Immunol, 2002, 23(11): 549-555.
[13]
Mosser DM, Edwards JP. Exploring the full spectrum of macrophage activation[J]. Nat Rev Immunol, 2008, 8(12): 958-969.
[14]
Vergadi E, Ieronymaki E, Lyroni K, et al. Akt signaling pathway in macrophage activation and M1/M2 polarization[J]. J Immunol, 2017, 198(3): 1006-1014.
[15]
Irelli A, Sirufo MM, Scipioni T, et al. mTOR Links tumor immunity and bone metabolism: What are the clinical implications?[J]. Int J Mol Sci, 2019, 20(23): 5841.
[16]
Liu H, Wu X, Gang N, et al. Macrophage functional phenotype can be consecutively and reversibly shifted to adapt to microenvironmental changes[J]. Int J Clin Exp Med, 2015, 8(2): 3044-3053.
[17]
Wang N, Liang H, Zen K. Molecular mechanisms that influence the macrophage m1-m2 polarization balance[J]. Front Immunol, 2014, 5: 614.
[18]
Ke X, Chen C, Song Y, et al. Hypoxia modififies the polarization of macrophages and their inflammatory microenvironment, and inhibits malignant behavior in cancer cells[J]. Oncol Lett, 2019, 18(6): 5871-5878.
[19]
Colegio OR, Chu NQ, Szabo AL, et al. Functional polarization of tumour-associated macrophages by tumour-derived lactic acid[J]. Nature, 2014, 513; 513, 559-563.
[20]
Ginaldi L, Di Benedetto MC, De Martinis M. Osteoporosis, inflflammation and ageing[J]. Immun Ageing, 2005, 2: 14.
[21]
Krzyszczyk P, Schloss R, Palmer A, et al. The role of macrophages in acute and chronic wound healing and interventions to promote pro-wound healing phenotypes[J]. Front Physiol, 2018, 9: 419.
[22]
Wynn TA, Vannella KM. Macrophages in tissue repair, regeneration, and fifibrosis[J]. Immunity, 2016, 44(3): 450-462.
[23]
Yang DH, Yang MY. The role of macrophage in the pathogenesis of osteoporosis[J]. Int J Mol Sci, 2019, 20(9): 2093.
[24]
Horwood NJ. Macrophage polarization and bone formation: a review[J]. Clin Rev Allergy Immunol, 2016, 51(1): 79-86.
[25]
Souza PP, Lerner UH. The role of cytokines in inflflammatory bone loss[J]. Immunol Investig, 2013, 42(7): 555-622.
[26]
Lind M, Deleuran B, Yssel, H, et al. IL-4 and ZL-13, but not IL-10, are chemotactic factors for human osteoblasts[J]. Cytokine, 1995, 7(1): 78-82.
[27]
Silfversward CJ, Frost A, Brandstrom H, et al. Interleukin-4 and interleukin-13 potentiate interleukin-1 induced secretion of interleukin-6 in human osteoblast-like cells[J]. J Orthop Res, 2004, 22(5): 1058-1062.
[28]
Palmqvist P, Lundberg P, Persson E, et al. Inhibition of hormone and cytokine-stimulated osteoclastogenesis and bone resorption by interleukin-4 and interleukin-13 is associated with increased osteoprotegerin and decreased rankl and rank in a stat6-dependent pathway[J]. J Biol Chem, 2006, 281(5): 2414-2429.
[29]
McGregor NE, Murat M, Elango J, et al. IL-6 exhibits both cis and trans signaling in osteocytes and osteoblasts, but only trans signaling promotes bone formation and osteoclastogenesis[J]. J Biol Chem, 2019, 294(19): 7850-7863.
[30]
Panagakos FS. Transforming growth factor-alpha stimulates chemotaxis of osteoblasts and osteoblast-like cells in vitro[J]. Biochem Mol Biol Int, 1994, 33(4): 643-650.
[31]
Sahoo A, Wali S, Nurieva R. T helper 2 and T follicular helper cells: regulation and function of interleukin-4[J]. Cytokine Growth Factor Rev, 2016, 30: 29-37.
[32]
Rath M, Müller I, Kropf P. Metabolism via arginase or nitric oxide synthase: two competing arginine pathways in macrophages[J]. Front Immunol, 2014, 5: 532.
[33]
Munder M. Arginase: an emerging key player in the mammalian immune system[J]. Br J Pharmacol, 2009, 158(3): 638-651.
[34]
Melo-Cardenas J, Bezavada L, Crawford JC, et al. IL-13/IL-4 signaling contributes to fibrotic progression of the myeloproliferative neoplasms[J]. Blood, 2022, 140(26): 2805-2817.
[35]
Osorio EY, Zhao W, Espitia C, et al. Progressive visceral leishmaniasis is driven by dominant parasite-induced STAT6 activation and STAT6-dependent host arginase 1 expression[J]. PLoS Pathog, 2012, 8(1): e1002417.
[36]
Muñoz J, Akhavan NS, Mullins AP, et al. Macrophage polarization and osteoporosis: a review[J]. Nutrients, 2020, 12(10): 2999.
[37]
Liu Q, Liu C, Yang Y, et al. Osteocyte-intrinsic mtorc1 signaling restrains trabecular bone accrual in mice[J]. J Cell Biochem, 2018, 119: 8743-8749.
[38]
Qu X, Mei J, Yu Z, et al. Lenalidomide regulates osteocytes fate and related osteoclastogenesis via IL-1β/NF-κB/RANKL signaling[J]. Biochem Biophys Res Commun, 2018, 501(2): 547-555.
[39]
Shukla P, Mansoori MN, Kakaji M, et al. Interleukin 27 (IL-27) alleviates bone loss in estrogen-defificient conditions by induction of early growth response-2 gene[J]. J Biol Chem, 2017, 292(11): 4686-4699.
[40]
Chhana A, Pool B, Callon KE, et al. Monosodium urate crystals reduce osteocyte viability and indirectly promote a shift in osteocyte function towards a proinflflammatory and proresorptive state[J]. Arthritis Res Ther, 2018, 20(1): 208.
[41]
Harmer D, Falank C, Reagan MR. Interleukin-6 interweaves the bone marrow microenvironment, bone loss, and multiple myeloma[J]. Front Endocrinol (Lausanne), 2019, 9: 788.
[42]
Sun W, Meednu N, Rosenberg A, et al. B cells inhibit bone formation in rheumatoid arthritis by suppressing osteoblast difffferentiation[J]. Nat Commun, 2018, 9(1): 5127.
[43]
Amarasekara DS, Yun H, Kim S, et al. Regulation of osteoclast differentiation by cytokine networks[J]. Immune Netw, 2018, 18(1): e8.
[44]
Gong L, Zhao Y, Zhang Y, et al. The macrophage polarization regulates msc osteoblast difffferentiation in vitro[J]. Ann Clin Lab Sci, 2016, 46(1): 65-71.
[45]
Zhang Y, Böse T, Unger RE, et al. Macrophage type modulates osteogenic difffferentiation of adipose tissue MSCs[J]. Cell Tissue Res, 2017, 369(2): 273-286.
[46]
Arabpour M, Saghazadeh A, Rezaei N. Anti-inflammatory and M2 macrophage polarization-promoting effect of mesenchymal stem cell-derived exosomes[J].Int Immunopharmacol, 2021, 97: 107823.
[47]
Moerman EJ, Teng K, Lipschitz DA, et al. Aging activates adipogenic and suppresses osteogenic programs in mesenchymal marrow stroma/stem cells: the role of PPAR-γ2 transcription factor and TGF-β/BMP signaling pathways[J]. Aging Cell, 2004, 3(6): 379-389.
[48]
Li CJ, Cheng P, Liang MK, et al. MicroRNA-188 regulates age-related switch between osteoblast and adipocyte differentiation[J]. J Clin Investig, 2015, 125(4): 1509-1522.
[49]
Hu L, Yin C, Zhao F, et al. Mesenchymal stem cells: cell fate decision to osteoblast or adipocyte and application in osteoporosis treatment[J]. Int J Mol Sci, 2018, 19(2): 360.
[50]
Jin H, Yao L, Chen K, et al. Evodiamine inhibits rankl-induced osteoclastogenesis and prevents ovariectomy-induced bone loss in mice[J]. J Cell Mol Med, 2019, 23(1): 522-534.
[51]
Kim B, Lee KY, Park B. Icariin abrogates osteoclast formation through the regulation of the rankl-mediated TRAF6/NF-κB/ERK signaling pathway in Raw264. 7 cells[J]. Phytomedicine, 2018, 51: 181-190.
[1] 张凯, 乔永杰, 林志强, 刘健, 邓泽群, 谭飞, 曾健康, 李嘉欢, 李培杰, 周胜虎. 假体周围骨溶解中巨噬细胞极化的机制研究进展[J/OL]. 中华关节外科杂志(电子版), 2024, 18(05): 618-625.
[2] 杨瑾, 刘雪克, 张媛媛, 金钧, 韦瑶. 肠道微生物来源石胆酸对脓毒症相关肝损伤的保护作用[J/OL]. 中华危重症医学杂志(电子版), 2024, 17(04): 265-274.
[3] 李璐璐, 马利红, 金佳佳, 谷伟. 干扰素基因刺激因子通过肺巨噬细胞胞葬功能调控急性肺损伤小鼠修复的研究[J/OL]. 中华危重症医学杂志(电子版), 2024, 17(02): 97-103.
[4] 薛嘉怡, 王丽, 艾涛. 巨噬细胞在儿童肺炎支原体肺炎中作用机制的研究现状[J/OL]. 中华妇幼临床医学杂志(电子版), 2023, 19(06): 643-648.
[5] 狄静怿, 陈禹江, 陈欣欣, 陈文霞. 基质细胞衍生因子1通过PI3K/AKT1信号通路对巨噬细胞极化的影响[J/OL]. 中华口腔医学研究杂志(电子版), 2024, 18(02): 89-95.
[6] 李卓骋, 陈羽翔, 高亮, 张宇, 朱许源, 马晓杰, 李涛, 赵甜甜, 蒋鸿涛. 巨噬细胞-肌成纤维细胞转化在肾纤维化过程中的作用[J/OL]. 中华移植杂志(电子版), 2024, 18(03): 181-185.
[7] 曹飞, 庞俊. 前列腺癌免疫微环境中免疫抑制性细胞分类及其作用机制[J/OL]. 中华腔镜泌尿外科杂志(电子版), 2024, 18(02): 121-125.
[8] 宋红霞, 杨英, 陈芳. 老年COPD患者并发骨质疏松症相关危险因素的研究进展[J/OL]. 中华肺部疾病杂志(电子版), 2023, 16(06): 895-898.
[9] 朱军, 宋家伟, 乔一桓, 郭雅婕, 刘帅, 姜玉, 李纪鹏. M2型巨噬细胞特征基因与结肠癌免疫微环境研究[J/OL]. 中华结直肠疾病电子杂志, 2024, 13(04): 303-311.
[10] 肖伍豪, 刘抗寒. 晚期慢性肾脏病患者骨质疏松症的治疗研究进展[J/OL]. 中华肾病研究电子杂志, 2024, 13(02): 92-96.
[11] 冉仁国, 罗政, 廖鑫, 张付民. 低频脉冲电磁场对骨质疏松性胸腰椎骨折内固定术后康复的促进作用[J/OL]. 中华老年骨科与康复电子杂志, 2024, 10(01): 39-45.
[12] 李松栗, 黄蔚, 巢杰, 杨毅, 邱海波. 单核/巨噬细胞来源的细胞外囊泡在急性呼吸窘迫综合征中的研究进展[J/OL]. 中华重症医学电子杂志, 2024, 10(03): 253-257.
[13] 陈含冰, 储翠林, 邱海波. 急性呼吸窘迫综合征中巨噬细胞死亡方式的研究进展[J/OL]. 中华重症医学电子杂志, 2024, 10(01): 79-84.
[14] 李仔祥, 王苏贵, 张先云, 卢建文, 嵇宏声, 姜福金. 肿瘤相关性巨噬细胞通过TNF-α/B7H3调节人膀胱癌细胞增殖的研究[J/OL]. 中华临床医师杂志(电子版), 2024, 18(01): 64-71.
[15] 邸文佳, 牛爱原. 基于东亚人群的肝硬化与骨质疏松症相关性研究[J/OL]. 中华老年病研究电子杂志, 2024, 11(01): 40-44.
阅读次数
全文


摘要


AI


AI小编
你好!我是《中华医学电子期刊资源库》AI小编,有什么可以帮您的吗?