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非编码RNA在子痫前期发病机制及临床应用中的研究进展

刘雅丽 沈瑶 吴兴琪 章锦曼

刘雅丽, 沈瑶, 吴兴琪, 章锦曼. 非编码RNA在子痫前期发病机制及临床应用中的研究进展[J]. 昆明医科大学学报.
引用本文: 刘雅丽, 沈瑶, 吴兴琪, 章锦曼. 非编码RNA在子痫前期发病机制及临床应用中的研究进展[J]. 昆明医科大学学报.
Yali LIU, Yao SHEN, Xingqi WU, Jinman ZHANG. Research Progress on Non-coding RNA in the Pathogenesis and Clinical Application of Preeclampsia[J]. Journal of Kunming Medical University.
Citation: Yali LIU, Yao SHEN, Xingqi WU, Jinman ZHANG. Research Progress on Non-coding RNA in the Pathogenesis and Clinical Application of Preeclampsia[J]. Journal of Kunming Medical University.

非编码RNA在子痫前期发病机制及临床应用中的研究进展

基金项目: 国家自然科学地区基金(82260645);云南省“兴滇英才支持计划”(XDYC-XLWS-2023-0074)
详细信息
    作者简介:

    刘雅丽(1994~),女,湖南株洲人,在读硕士研究生,住院医师,主要从事妇产科、子痫前期临床及研究工作

    通讯作者:

    章锦曼,E-mail:171887587@qq.com

  • 中图分类号: R714.2

Research Progress on Non-coding RNA in the Pathogenesis and Clinical Application of Preeclampsia

  • 摘要: 子痫前期(preeclampsia,PE)是一种病因未明、严重威胁母婴健康的妊娠期并发症,且缺乏有效的早期预测与防治手段。系统归纳了微小RNA(microRNA,miRNA)、长链非编码RNA(long non-coding RNA,lncRNA)和环状RNA(circular RNA,circRNA)三类ncRNA的最新研究进展,重点阐述它们通过构成复杂的调控网络,影响滋养细胞功能、胎盘血管重塑、母胎界面免疫炎症及氧化应激等多个关键环节,从而驱动PE发生发展的具体机制。同时总结ncRNA作为新型生物标志物和治疗靶点的巨大临床应用潜力,并深入探讨当前临床转化所面临的主要挑战与未来研究方向,以期为PE的精准防控提供理论依据与创新思路。
  • 图  1  三种ncRNA在子痫前期中的作用机制

    Figure  1.  Mechanistic diagram of the roles of three ncRNAs in preeclampsia

    图  2  三种ncRNA在子痫前期中的协同调控网络机制

    Figure  2.  Cooperative regulatory network mechanisms of three ncRNAs in preeclampsia

    表  1  微小RNA(miRNA)在子痫前期中的变化、机制及临床应用的相关研究

    Table  1.   Studies on the alterations,mechanisms,and clinical applications of microRNAs (miRNAs) in preeclampsia

    编号 研究者、
    文献
    发表年份 ncRNA 来源
    (胎盘
    外周血)
    表达结果 靶点(通路、蛋白) 功能 潜在临床价值
    1 Misa[10] 2023 miR-515-5p 血清 XIAP 抑制了EVT的增殖和侵袭 发病机制、预测、
    治疗
    2 Luo[31] 2024 miR-190a-3p 胎盘 DAPK1 促进EVT的自噬 发病机制
    3 Wu、Luo[21] 2024 miR-141-3p 胎盘 NLRP3、CXCR4、LC3、DUSP1、TAB2/TAK1 抑制EVT的活力、侵袭、自噬和和子宫螺旋动脉重塑 发病机制、诊断
    4 Polina[24] 2024 miR-27a-3p、miR-27a-5p 胎盘 TGFβR2 诱发免疫炎症异常 发病机制
    5 Jaber[32] 2024 miR-203a-3p 血清 IL-24 抑制炎症免疫异常 发病机制、治疗
    6 Illarionov
    [2526]
    2024 MiR-223-3p 尿液 NLRP3、IL-1β、
    IL-18
    抑制炎症免疫异常 发病机制、预测诊断
    7 Liu[30] 2024 MiR-195-5p 血清 OTX1、VEGFA、MAPK 对胎盘损伤和氧化应激的保护作用 发病机制、治疗
    8 Cen[1416] 2025 miR-144-5、miR-486-5p 外周血 ARHGAP5、
    E-钙粘蛋白
    促进EVT的迁移和侵袭 发病机制、治疗
    9 Wei[20] 2025 miR-34a-5p 外周血 METTL14 抑制胎盘螺旋动脉的生成 发病机制
      注:XIAP:X连锁凋亡抑制蛋白;DAPK1:死亡相关蛋白激酶1;NLRP3:NOD样受体热蛋白结构域相关蛋白3;CXCR4 :CXC趋化因子受体4型;LC3 :微管相关蛋白1轻链3;DUSP1:双特异性磷酸酶1;TAB2/TAK1:TAK1结合蛋白2 / TGF-β激活激酶1 ;TGFβR2:转化生长因子-β受体2型;OTX1:正交opedia同源框1;VEGFA :血管内皮生长因子A;MAPK:丝裂原活化蛋白激酶;ARHGAP5:Rho GTP酶激活蛋白5;METTL14:甲基转移酶样14。
    下载: 导出CSV

    表  2  LncRNA在子痫前期中的变化、机制及临床应用的相关研究

    Table  2.   Studies on alterations,mechanisms,and clinical applications of lncRNAs in preeclampsia

    编号研究者、
    文献
    发表年份LncRNA来源
    表达结果
    靶点(通路、蛋白)功能潜在临床价值
    1Wang[39]2023lncRNA GHET1胎盘EZH2/LSD1/MT2A抑制EVT的增殖、迁移和侵袭发病机制、预测诊断
    2Wang[36]2023lncRNA HOXD-AS1胎盘METTL3/miR-135a/
    β-TRCP
    抑制EVT的侵袭和迁移,促进EVT凋亡和炎症免疫失调发病机制
    3Lekva[46]2023lncRNA TUG1外周血的白细胞-抗炎作用减弱、铁稳态失衡发病机制、预测诊断
    4Ding[47]2024LncRNA PDIA3P1胎盘SFRP1阻碍EVT的增殖、侵袭和迁移发病机制、治疗
    5Jiang[46]2024LncRNA-NEAT1胎盘miR-217/Wnt3/
    β-catenin
    抑制EVT增殖、迁移和侵入发病机制
    6Feng、Nie
    [4243]
    2021、2024lncRNA MALAT1胎盘miR-133a-3p/ CORO1C抑制滋EVT增殖、侵袭、迁移和胎盘血管形成发病机制、预测诊断
    7Yong[44]2024LncRNA AC092100.1胎盘YTHDC2/VEGFA抑制血管生成发病机制、治疗
    8Song[37]2024LncRNA UCA1胎盘miRNA-18a/
    缺氧诱导因子-1α
    促进EVT迁移、侵袭和增殖发病机制、阿司匹林预防的机制
    9Zhang[40]2025lncRNA-ATB胎盘PABPC1/p53/MDM2抑制了EVT的增殖、迁移、侵袭和管形成,增强细胞凋亡发病机制、治疗
    10Wu[48]2025LncRNA SNHG15胎盘miR-451a/ATF2抑制了EVT的增殖,迁移和侵袭发病机制
      注:METTL3:甲基转移酶样3;β-TRCP:β-转导重复相容蛋白;SFRP1:分泌型卷曲相关蛋白1;Wnt3:MMTV整合位点家族成员3;CORO1C:冠蛋白1C;YTHDC2:YTH结构域包含蛋白2;VEGFA:血管内皮生长因子A;PABPC1:多聚腺苷酸结合蛋白胞质1;MDM2:鼠双微体2蛋白;ATF2:激活转录因子2 。
    下载: 导出CSV

    表  3  CircRNA在子痫前期中的变化、机制及临床应用的相关研究

    Table  3.   Studies on alterations,mechanisms,and clinical applications of CircRNAs in preeclampsia

    编号 研究者、
    文献
    发表年份 CircRNA 来源 表达结果 靶点(通路、蛋白) 功能 潜在临床价值
    1 Wu[66] 2023 circPTK2 血样 miR-619/WNT7B 抑制EVT的增殖、迁移和侵袭 诊断、治疗
    2 Zhou[67] 2023 circ_0002348 血样 miR-126-3p/BAK1 促进EVT的凋亡,抑制增殖 诊断、治疗
    3 Song[68] 2023 circ_0001326 血样 miR-145-5p/TGFB2 抑制EVT的活力、迁移和侵袭 发病机制
    4 Lu[58] 2023 Circ SGK1 胎盘组织 miR-508-3p/PUM1 抑制EVT的生长和抗氧化分子以及血管生成 发病机制
    5 Xiong[5152] 2023 circRNA_0088196 胎盘组织 miR-379-5p/HSPA5 促进EVT凋亡并抑制其增殖 发病机制
    6 Wang[59] 2023 circ_0015382 胎盘组织 miR-616-3p/THBS2 抑制EVT增殖、迁移、侵袭和胎盘的血管生成能力 发病机制、诊断
    7 Song[50] 2024 circ_0007611 血样 miR-34c-5p/LPAR2 阻碍EVT的增殖,促进其凋亡 发病机制、诊断
    8 Li[60] 2024 circ_0003314 胎盘组织 miR-26b-5p/IL1RAP 抑制EVT增殖、迁移、侵袭和血管生成,诱导细胞凋亡 发病机制、诊断
    9 Wu[69] 2024 circHIPK3 胎盘组织 miR-124-3p/CPT1A 抑制内皮细胞脂肪酸氧化活性、细胞增殖和血管形成 发病机制、治疗
    10 Shao[70] 2024 circ_0022707 胎盘组织 miR-3135b/GHR/
    PI3K/Akt
    促进EVT增殖和细胞周期进展,同时抑制细胞凋亡 发病机制、治疗
    11 Su[54] 2025 circ-Hdac4 胎盘组织 miR-30c/RBPJ 胎盘功能障碍:胎儿数量、体重和胎盘重量减少 发病机制、
    预测、治疗
      注:WNT7B:MMTV整合位点家族成员7B ;BAK1:Bcl-2同源拮抗/杀伤因子1;TGFB2:转化生长因子β2;PUM1:Pumilio同源RNA结合蛋白1;HSPA5:热休克蛋白家族A成员5;THBS2:血小板反应蛋白2 ;LPAR2:溶血磷脂酸受体2;IL1RAP:白细胞介素1受体辅助蛋白;GHR:生长激素受体 ;CPT1A:肉碱棕榈酰转移酶1A;PI3K:磷脂酰肌醇3-激酶 ;Akt:蛋白激酶B;RBPJ:重组信号结合蛋白Jκ。
    下载: 导出CSV
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