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中华老年病研究电子杂志 ›› 2022, Vol. 09 ›› Issue (03) : 51 -55. doi: 10.3877/cma.j.issn.2095-8757.2020.03.012

综述

microRNA与老年性骨关节炎
李锡勇1, 杨溯1, 张雄杰1, 李松风1, 韩鹏飞2,()   
  1. 1. 046000 山西省长治医学院研究生处
    2. 046000 长治,长治医学院附属和平医院骨科
  • 收稿日期:2022-03-15 出版日期:2022-08-28
  • 通信作者: 韩鹏飞
  • 基金资助:
    山西省卫生健康委员会基金项目(2020133)

Research progress on microRNA in the treatment of senile osteoarthritis

Xiyong Li1, Su Yang1, Xiongjie Zhang1, Songfeng Li1, Pengfei Han2,()   

  1. 1. School of Postgraduate Student, Changzhi Medical College, Changzhi 046000, China
    2. Department of Orthopaedics, Heping Hospital Affiliated to Changzhi Medical College, Changzhi 046000, China
  • Received:2022-03-15 Published:2022-08-28
  • Corresponding author: Pengfei Han
引用本文:

李锡勇, 杨溯, 张雄杰, 李松风, 韩鹏飞. microRNA与老年性骨关节炎[J/OL]. 中华老年病研究电子杂志, 2022, 09(03): 51-55.

Xiyong Li, Su Yang, Xiongjie Zhang, Songfeng Li, Pengfei Han. Research progress on microRNA in the treatment of senile osteoarthritis[J/OL]. Chinese Journal of Geriatrics Research(Electronic Edition), 2022, 09(03): 51-55.

骨关节炎是老年人群最常见的关节疾病之一,其发病机制至今仍未阐明。microRNA是一种负性调控基因表达的小双链RNA,通过参与信号通路转导以及细胞凋亡、衰老、自体吞噬等生物学过程,在软骨细胞的分化、发育和稳态中发挥着关键作用。大量研究表明,正常关节软骨和老年性骨关节炎软骨细胞中多个microRNA的表达存在差异,且在动物模型中关节腔内传递治疗性microRNA已被证明可以减轻老年性骨关节炎,因此某些特定microRNA已被认为可作为老年性骨关节炎的循环生物标志物和新的治疗策略。但限于各研究群体和数量的差异,以及检测方法和范围的差异,研究结果尚需进一步验证,如何将其转化为老年性骨关节炎的治疗手段将是下一步的研究重点。

Osteoarthritis is one of the most common joint diseases in the elderly, but there are still many unresolved problems in the detailed pathogenesis. MicroRNA are small double-stranded RNA that negatively regulate gene expression, and play a key role in the differentiation, development and homeostasis of chondrocytes by participating in biological processes such as signaling pathway transduction, apoptosis and senescence, and autophagy. Numerous studies have shown that there are significant differences in the expression of microRNA in normal articular cartilage and senile osteoarthritis chondrocytes, and in animal models, intra-articular delivery of therapeutic microRNA has been shown to alleviate senile osteoarthritis, so some specific microRNA have been proposed as a circulating biomarker and novel therapeutic strategy for senile osteoarthritis. However, due to the differences in the groups and numbers of patients in each study, as well as the differences in the methods and scope of detection techniques, the results still need to be further verified. How to transform it into the treatment of senile osteoarthritis will be the next research focus in the future.

图1 microRNA生物合成示意图
[1]
许成燕,陈军香,王教明,等.中国人群膝骨关节炎危险因素的Meta分析[J].中国循证医学杂志202121(7):772-778.
[2]
张莹莹,李旭东,杨佳娟,等.中国40岁及以上人群骨关节炎患病率的Meta分析[J].中国循证医学杂志202121(4):407-414.
[3]
Vina ER, Kwoh CK. Epidemiology of osteoarthritis: Literature update[J]. Curr Opin Rheumatol, 2018, 30(2):160-167.
[4]
申延清,刘风霞,曹红,等.膝骨关节炎患者的临床表现及相关影响因素[J].中国组织工程研究与临床康复201115(9):1643-1646.
[5]
Fittipaldi S, Visconti VV, Tarantino U, et al. Genetic variability in noncoding RNAs: Involvement of miRNAs and long noncoding RNAs in osteoporosis pathogenesis[J]. Epigenomics, 2020, 12(22):2035-2049.
[6]
Sibley CR, Seow Y, Saayman S, et al. The biogenesis and characterization of mammalian miRs of mirtron origin[J]. Nucleic Acids Res, 2012, 40(1):438-448.
[7]
Shvedova M, Kobayashi T. MiRs in cartilage development and dysplasia[J]. Bone, 2020, 140:115564.
[8]
Barter MJ, Tselepi M, Gómez R, et al. Genome-wide miR and gene analysis of mesenchymal stem cell chondrogenesis identifies an essential role and multiple targets for miR-140-5p[J]. Stem Cells, 2015, 33(11):3266-3280.
[9]
Tao SC, Yuan T, Zhang YL, et al. Exosomes derived from miR-140-5p-overexpressing human synovial mesenchymal stem cells enhance cartilage tissue regeneration and prevent osteoarthritis of the knee in a rat model[J]. Theranostics, 2017, 7(1):180-195.
[10]
Yang J, Qin S, Yi C, et al. MiR-140 is co-expressed with Wwp2-C transcript and activated by Sox9 to target Sp1 in maintaining the chondrocyte proliferation[J]. FEBS Letters, 2011, 585(19):2992-2997.
[11]
Chen W, Chen L, Zhang Z, et al. MiR-455-3p modulates cartilage development and degeneration through modification of histone H3 acetylation[J]. Biochim Biophys Acta, 2016, 1863(12):2881-2891.
[12]
Sun H, Zhao X, Zhang C, et al. MiR-455-3p inhibits the degenerate process of chondrogenic differentiation through modification of DNA methylation[J]. Cell Death Dis, 2018, 9(5):537.
[13]
Miyaki S, Sato T, Inoue A, et al. MiR-140 plays dual roles in both cartilage development and homeostasis[J]. Genes Dev, 2010, 24(11):1173-1185.
[14]
Chen G, Gao X, Wang J, et al. Hypoxia-induced miR-146a represses Bcl-2 through Traf6/IRAK1 but not Smad4 to promote chondrocyte autophagy[J]. Biol Chem, 2017, 398(4):499-507.
[15]
Zhang F, Wang J, Chu J, et al. MiR-146a induced by hypoxia promotes chondrocyte autophagy through Bcl-2[J]. Cell Physiol Biochem, 2015, 37(4):1442-1453.
[16]
Liu JN, Lu S, Fu CM. MiR-146a expression profiles in osteoarthritis in different tissue sources: A meta-analysis of observational studies[J]. J Orthop Surg Res, 2022, 17:148.
[17]
Zhang X, Wang C, Zhao J, et al. miR-146a facilitates osteoarthritis by regulating cartilage homeostasis via targeting Camk2d and Ppp3r2[J/OL]. Cell Death Dis, 2017, 8(4):e2734.
[18]
Guan YJ, Li J, Yang X, et al. Evidence that miR-146a attenuates aging- and trauma-induced osteoarthritis by inhibiting Notch1, IL-6, and IL-1 mediated catabolism[J/OL]. Aging Cell, 2018, 17(3):e12752.
[19]
Yan S, Wang M, Zhao J, et al. MiR-34a affects chondrocyte apoptosis and proliferation by targeting the SIRT1/p53 signaling pathway during the pathogenesis of osteoarthritis[J]. Int J Mol Med, 2016, 38(1):201-209.
[20]
Zhang W, Hsu P, Zhong B, et al. MiR-34a enhances chondrocyte apoptosis, senescence and facilitates development of osteoarthritis by targeting DLL1 and regulating PI3K/AKT pathway[J]. Cell Physiol Biochem, 2018, 48(3):1304-1316.
[21]
Philipot D, Guérit D, Platano D, et al. p16INK4a and its regulator miR-24 link senescence and chondrocyte terminal differentiation-associated matrix remodeling in osteoarthritis[J]. Arthritis Res Ther, 2014, 16(1):R58.
[22]
Zhao X, Wang T, Cai B, et al. MiR-495 enhances chondrocyte apoptosis, senescence and promotes the progression of osteoarthritis by targeting AKT1[J]. Am J Transl Res, 2019, 11(4):2232-2244.
[23]
Yang DW, Qian GB, Jiang MJ, et al. Inhibition of miR-495 suppresses chondrocyte apoptosis through activation of the NF-κB signaling pathway by regulating CCL4 in osteoarthritis[J]. Gene Ther, 2019, 26(6): 217-229.
[24]
Lian WS, Ko JY, Wu RW, et al. MiR-128a represses chondrocyte autophagy and exacerbates knee osteoarthritis by disrupting Atg12[J]. Cell Death Dis, 2018, 9(9):919.
[25]
Le LTT, Swingler TE, Crowe N, et al. The miR-29 family in cartilage homeostasis and osteoarthritis[J]. Mol Med (Berl), 2016, 94(5):583-596.
[26]
Hu S, Zhao X, Mao G, et al. MiR-455-3p promotes TGF-β signaling and inhibits osteoarthritis development by directly targeting PAK2[J]. Exp Mol Med, 2019, 51(10):1-13.
[27]
Anderson BA, McAlinden A. miR-483 targets SMAD4 to suppress chondrogenic differentiation of human mesenchymal stem cells[J]. J Orthop Res, 2017, 35(11):2369-2377.
[28]
Wang H, Zhang H, Sun Q, et al. Chondrocyte mTORC1 activation stimulates miR-483-5p via HDAC4 in osteoarthritis progression[J]. J Cell Physiol, 2019, 234(3):2730-2740.
[29]
Cong L, Zhu Y, Tu G. A bioinformatic analysis of miRs role in osteoarthritis[J]. Osteoarthritis Cartilage, 2017, 25(8):1362-1371.
[30]
Coutinho de Almeida R, Ramos YFM, Mahfouz A, et al. RNA sequencing data integration reveals an miRNA interactome of osteoarthritis cartilage[J]. Ann Rheum Dis, 2019, 78(2):270-277.
[31]
Beyer C, Zampetaki A, Lin NY, et al. Signature of circulating miRs in osteoarthritis[J/OL]. Ann Rheum Dis, 2015, 74(3):e18.
[32]
Kong R, Gao J, Si Y, et al. Combination of circulating miR-19b-3p, miR-122-5p and miR-486-5p expressions correlates with risk and disease severity of knee osteoarthritis[J]. Am J Transl Res, 2017, 9(6):2852-2864.
[33]
Ntoumou E, Tzetis M, Braoudaki M, et al. Serum miR array analysis identifies miR-140-3p, miR-33b-3p and miR-671-3p as potential osteoarthritis biomarkers involved in metabolic processes[J]. Clin Epigenetics, 2017, 9:127.
[34]
Wan L, Zhao Q, Niu G, et al. Plasma miR-136 can be used to screen patients with knee osteoarthritis from healthy controls by targeting IL-17[J]. Exp Ther Med, 2018, 16(4):3419-3424.
[35]
Xia S, Tian H, Fan L, et al. Peripheral blood miR-181-5p serves as a marker for screening patients with osteoarthritis by targeting TNFα[J]. Clin Lab, 2017, 63(11):1819-1825.
[36]
Zhou Z, Tian F, An N, et al. MiR-300 serves as potential biomarker to screen knee osteoarthritis patients by targeting TNFα[J]. Clin Lab, 2018, 64(4): 577-584.
[37]
Latifkar A, Hur YH, Sanchez JC, et al. New insights into extracellular vesicle biogenesis and function[J]. J Cell Sci, 2019, 132(13):jcs222406.
[38]
Mao G, Zhang Z, Hu S, et al. Exosomes derived from miR-92a-3p-overexpressing human mesenchymal stem cells enhance chondrogenesis and suppress cartilage degradation via targeting WNT5A[J]. Stem Cell Res Ther, 2018, 9(1):247.
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