+高级检索
首页 > 优先出版
PDF HTML阅读 XML下载 导出引用 引用提醒
血管平滑肌细胞表型转换与细胞焦亡在腹主动脉瘤中的作用及研究进展
作者:
作者单位:

1.河北医科大学研究生学院;2.河北北方学院研究生学院;3.华北理工大学研究生院;4.河北医科大学基础医学院生化研究室;5.河北省人民医院临床医学研究中心

基金项目:

] 国家自然科学(82270508)；河北省自然科学基金联合(H2024307005)；神经与血管生物学教育部重点实验室主任基金青年(NV20210006)；河北省人社厅重点研发计划项目(A202105015)


Vascular smooth muscle cell phenotype switch and Cell pyroptosis in the role and research progress of Abdominal aortic aneurysm
Author:
Affiliation:

1.Graduate School of Hebei Medical University;2.Graduate School of Hebei North University;3.Graduate School, North China University of Science and Technology;4.Department of Biochemistry, School of Basic Medicine, Hebei Medical University;5.Clinical Medicine Research Cener, Hebei General Hospital

  • 摘要
    • | |
  • 访问统计
    • |
  • 参考文献 [49]
    • |
  • 相似文献
    • | | |
  • 文章评论
    摘要:

    腹主动脉瘤(Abdominal aortic aneurysm,AAA)作为一种隐匿型致死性疾病,其背后的发展机制尚不清楚。研究已经发现血管平滑肌细胞(Vascular Smooth Muscle Cell,VSMCs )表型转换和细胞焦亡(Cell pyroptosis)是与AAA产生发展密切相关的两种生物学过程,可能会成为揭示AAA发生机制的重要学说,为AAA的诊断和治疗提供新的方向。本文将通过介绍VSMCs表型转换和细胞焦亡与AAA之间的调控关系展开论述。

    Abstract:

    Abdominal aortic aneurysm (AAA) is a hidden and fatal disease, but its underlying developmental mechanism remains unclear. It has been found that phenotypic switching of vascular smooth muscle cells and pyroptosis are two biological processes closely related to the appearance and progress of AAA, which may become an important theory to reveal the mechanism of AAA and provide a new direction for the diagnosis and treatment of AAA. In this review, we will discuss the phenotypic switch of VSMCs and the regulatory relationship between cell pyroptosis and AAA.

    参考文献
    [1] GOLLEDGE J. Abdominal aortic aneurysm: update on pathogenesis and medical treatments [J]. Nature reviews Cardiology, 2019, 16(4): 225-42.
    [2] DAVIS F M, DAUGHERTY A, LU H S. Updates of Recent Aortic Aneurysm Research [J]. Arteriosclerosis, thrombosis, and vascular biology, 2019, 39(3): e83-e90.
    [3] GALLITTO E, SOBOCINSKI J, MASCOLI C, et al. Fenestrated and Branched Thoraco-abdominal Endografting after Previous Open Abdominal Aortic Repair [J]. European journal of vascular and endovascular surgery : the official journal of the European Society for Vascular Surgery, 2020, 60(6): 843-52.
    [4] LAI C H, CHANG C W, LEE F T, et al. Targeting vascular smooth muscle cell dysfunction with xanthine derivative KMUP-3 inhibits abdominal aortic aneurysm in mice [J]. Atherosclerosis, 2020, 297: 16-24.
    [5] QIAN G, ADEYANJU O, OLAJUYIN A, et al. Abdominal Aortic Aneurysm Formation with a Focus on Vascular Smooth Muscle Cells [J]. Life (Basel, Switzerland), 2022, 12(2).
    [6] NEWTON K, DIXIT V M, KAYAGAKI N. Dying cells fan the flames of inflammation [J]. Science (New York, NY), 2021, 374(6571): 1076-80.
    [7] YU P, ZHANG X, LIU N, et al. Pyroptosis: mechanisms and diseases [J]. Signal transduction and targeted therapy, 2021, 6(1): 128.
    [8] FU H, SHEN Q R, ZHAO Y, et al. Activating α7nAChR ameliorates abdominal aortic aneurysm through inhibiting pyroptosis mediated by NLRP3 inflammasome [J]. Acta pharmacologica Sinica, 2022, 43(10): 2585-95.
    [9] CAO G, XUAN X, HU J, et al. How vascular smooth muscle cell phenotype switching contributes to vascular disease [J]. Cell communication and signaling : CCS, 2022, 20(1): 180.
    [10] OH S, SON M, PARK C H, et al. Pyrogallol-Phloroglucinol-6,6-Bieckolon Attenuates Vascular Smooth Muscle Cell Proliferation and Phenotype Switching in Hyperlipidemia through Modulation of Chemokine Receptor 5 [J]. Marine drugs, 2020, 18(8).
    [11] TIERNEY J W, EVANS B C, CHEUNG-FLYNN J, et al. Therapeutic MK2 inhibition blocks pathological vascular smooth muscle cell phenotype switch [J]. JCI insight, 2021, 6(19).
    [12] HE X, LIAN Z, YANG Y, et al. Long Non-coding RNA PEBP1P2 Suppresses Proliferative VSMCs Phenotypic Switching and Proliferation in Atherosclerosis [J]. Molecular therapy Nucleic acids, 2020, 22: 84-98.
    [13] HE X, DENG J, YU X J, et al. Activation of M3AChR (Type 3 Muscarinic Acetylcholine Receptor) and Nrf2 (Nuclear Factor Erythroid 2-Related Factor 2) Signaling by Choline Alleviates Vascular Smooth Muscle Cell Phenotypic Switching and Vascular Remodeling [J]. Arteriosclerosis, thrombosis, and vascular biology, 2020, 40(11): 2649-64.
    [14] LIANG M, CAI Z, JIANG Y, et al. SENP2 Promotes VSMC Phenotypic Switching via Myocardin De-SUMOylation [J]. International journal of molecular sciences, 2022, 23(20).
    [15] WANG Y, DONG C Q, PENG G Y, et al. MicroRNA-134-5p Regulates Media Degeneration through Inhibiting VSMC Phenotypic Switch and Migration in Thoracic Aortic Dissection [J]. Molecular therapy Nucleic acids, 2019, 16: 284-94.
    [16] FARINA F M, HALL I F, SERIO S, et al. miR-128-3p Is a Novel Regulator of Vascular Smooth Muscle Cell Phenotypic Switch and Vascular Diseases [J]. Circulation research, 2020, 126(12): e120-e35.
    [17] ZHANG M, LI F, WANG X, et al. MiR-145 alleviates Hcy-induced VSMC proliferation, migration, and phenotypic switch through repression of the PI3K/Akt/mTOR pathway [J]. Histochemistry and cell biology, 2020, 153(5): 357-66.
    [18] CAO Y, CAO Z, WANG W, et al. MicroRNA?199a?5p regulates FOXC2 to control human vascular smooth muscle cell phenotypic switch [J]. Molecular medicine reports, 2021, 24(3).
    [19] WANG W, WANG Y, PIAO H, et al. Bioinformatics Analysis Reveals MicroRNA-193a-3p Regulates ACTG2 to Control Phenotype Switch in Human Vascular Smooth Muscle Cells [J]. Frontiers in genetics, 2020, 11: 572707.
    [20] ZENG Z, XIA L, FAN S, et al. Circular RNA CircMAP3K5 Acts as a MicroRNA-22-3p Sponge to Promote Resolution of Intimal Hyperplasia Via TET2-Mediated Smooth Muscle Cell Differentiation [J]. Circulation, 2021, 143(4): 354-71.
    [21] RONG Z H, CHANG N B, YAO Q P, et al. Suppression of circDcbld1 Alleviates Intimal Hyperplasia in Rat Carotid Artery by Targeting miR-145-3p/Neuropilin-1 [J]. Molecular therapy Nucleic acids, 2019, 18: 999-1008.
    [22] HALL I F, CLIMENT M, QUINTAVALLE M, et al. Circ_Lrp6, a Circular RNA Enriched in Vascular Smooth Muscle Cells, Acts as a Sponge Regulating miRNA-145 Function [J]. Circulation research, 2019, 124(4): 498-510.
    [23] WANG Z, LIU B, ZHU J, et al. Nicotine-mediated autophagy of vascular smooth muscle cell accelerates atherosclerosis via nAChRs/ROS/NF-κB signaling pathway [J]. Atherosclerosis, 2019, 284: 1-10.
    [24] HU C, HUANG W, XIONG N, et al. SP1-mediated transcriptional activation of PTTG1 regulates the migration and phenotypic switching of aortic vascular smooth muscle cells in aortic dissection through MAPK signaling [J]. Archives of biochemistry and biophysics, 2021, 711: 109007.
    [25] BRANGSCH J, REIMANN C, KAUFMANN J O, et al. Concurrent Molecular Magnetic Resonance Imaging of Inflammatory Activity and Extracellular Matrix Degradation for the Prediction of Aneurysm Rupture [J]. Circulation Cardiovascular imaging, 2019, 12(3): e008707.
    [26] QUINTANA R A, TAYLOR W R. Cellular Mechanisms of Aortic Aneurysm Formation [J]. Circulation research, 2019, 124(4): 607-18.
    [27] MALECKI C, HAMBLY B D, JEREMY R W, et al. The Role of Inflammation and Myeloperoxidase-Related Oxidative Stress in the Pathogenesis of Genetically Triggered Thoracic Aortic Aneurysms [J]. International journal of molecular sciences, 2020, 21(20).
    [28] ZHOU Z, ZHOU H, ZOU X, et al. RUNX3 is up-regulated in abdominal aortic aneurysm and regulates the function of vascular smooth muscle cells by regulating TGF-β1 [J]. Journal of molecular histology, 2022, 53(1): 1-11.
    [29] JIANG B, WANG M, LI X, et al. Hexarelin attenuates abdominal aortic aneurysm formation by inhibiting SMC phenotype switch and inflammasome activation [J]. Microvascular research, 2022, 140: 104280.
    [30] LU W, ZHOU Y, ZENG S, et al. Loss of FoxO3a prevents aortic aneurysm formation through maintenance of VSMC homeostasis [J]. Cell death disease, 2021, 12(4): 378.
    [31] SHI X, MA W, PAN Y, et al. MiR-126-5p promotes contractile switching of aortic smooth muscle cells by targeting VEPH1 and alleviates Ang II-induced abdominal aortic aneurysm in mice [J]. Laboratory investigation; a journal of technical methods and pathology, 2020, 100(12): 1564-74.
    [32] SI X, CHEN Q, ZHANG J, et al. MicroRNA-23b prevents aortic aneurysm formation by inhibiting smooth muscle cell phenotypic switching via FoxO4 suppression [J]. Life sciences, 2022, 288: 119092.
    [33] WANG X, LI H, LI W, et al. The role of Caspase-1/GSDMD-mediated pyroptosis in Taxol-induced cell death and a Taxol-resistant phenotype in nasopharyngeal carcinoma regulated by autophagy [J]. Cell biology and toxicology, 2020, 36(5): 437-57.
    [34] FRANK D, VINCE J E. Pyroptosis versus necroptosis: similarities, differences, and crosstalk [J]. Cell death and differentiation, 2019, 26(1): 99-114.
    [35] WRIGHT S S, VASUDEVAN S O, RATHINAM V A. Mechanisms and Consequences of Noncanonical Inflammasome-Mediated Pyroptosis [J]. Journal of molecular biology, 2022, 434(4): 167245.
    [36] WANG M, JIANG S, ZHANG Y, et al. The Multifaceted Roles of Pyroptotic Cell Death Pathways in Cancer [J]. Cancers, 2019, 11(9).
    [37] DAI Z, LIU W C, CHEN X Y, et al. Gasdermin D-mediated pyroptosis: mechanisms, diseases, and inhibitors [J]. Frontiers in immunology, 2023, 14: 1178662.
    [38] JIANG K, TU Z, CHEN K, et al. Gasdermin D inhibition confers antineutrophil-mediated cardioprotection in acute myocardial infarction [J]. The Journal of clinical investigation, 2022, 132(1).
    [39] SHI H, GAO Y, DONG Z, et al. GSDMD-Mediated Cardiomyocyte Pyroptosis Promotes Myocardial I/R Injury [J]. Circulation research, 2021, 129(3): 383-96.
    [40] WEI S, FENG M, ZHANG S. Molecular Characteristics of Cell Pyroptosis and Its Inhibitors: A Review of Activation, Regulation, and Inhibitors [J]. International journal of molecular sciences, 2022, 23(24).
    [41] LI Z, GUO J, BI L. Role of the NLRP3 inflammasome in autoimmune diseases [J]. Biomedicine pharmacotherapy = Biomedecine pharmacotherapie, 2020, 130: 110542.
    [42] ZENG C, WANG R, TAN H. Role of Pyroptosis in Cardiovascular Diseases and its Therapeutic Implications [J]. International journal of biological sciences, 2019, 15(7): 1345-57.
    [43] KESAVARDHANA S, MALIREDDI R K S, KANNEGANTI T D. Caspases in Cell Death, Inflammation, and Pyroptosis [J]. Annual review of immunology, 2020, 38: 567-95.
    [44] ZHAOLIN Z, GUOHUA L, SHIYUAN W, et al. Role of pyroptosis in cardiovascular disease [J]. Cell proliferation, 2019, 52(2): e12563.
    [45] LIAO F, WANG L, WU Z, et al. Disulfiram protects against abdominal aortic aneurysm by ameliorating vascular smooth muscle cells pyroptosis [J]. Cardiovascular drugs and therapy, 2022.
    [46] WORTMANN M, SKORUBSKAYA E, PETERS A S, et al. Necrotic cell debris induces a NF-κB-driven inflammasome response in vascular smooth muscle cells derived from abdominal aortic aneurysms (AAA-SMC) [J]. Biochemical and biophysical research communications, 2019, 511(2): 343-9.
    [47] USUI F, SHIRASUNA K, KIMURA H, et al. Inflammasome activation by mitochondrial oxidative stress in macrophages leads to the development of angiotensin II-induced aortic aneurysm [J]. Arteriosclerosis, thrombosis, and vascular biology, 2015, 35(1): 127-36.
    [48] GAO J, CHEN Y, WANG H, et al. Gasdermin D Deficiency in Vascular Smooth Muscle Cells Ameliorates Abdominal Aortic Aneurysm Through Reducing Putrescine Synthesis [J]. Advanced science (Weinheim, Baden-Wurttemberg, Germany), 2023, 10(5): e2204038.
    [49] BURGER F, BAPTISTA D, ROTH A, et al. NLRP3 Inflammasome Activation Controls Vascular Smooth Muscle Cells Phenotypic Switch in Atherosclerosis [J]. International journal of molecular sciences, 2021, 23(1).
    相似文献
    引证文献
    网友评论
    网友评论
    分享到微博
    发 布
引用本文

复制
分享
文章指标
  • 点击次数:116
  • 下载次数: 0
  • HTML阅读次数: 0
  • 引用次数: 0
历史
  • 收稿日期:2024-05-07
  • 最后修改日期:2024-10-01
  • 录用日期:2024-10-25
您是第8863702 位访问者
版权所有:中国比较医学杂志 主管单位：中国科学技术协会 主办单位：中国实验动物学会 中国医学科学院医学实验动物研究所
地址：北京市朝阳区潘家园南里5号 邮 编 ：100021 电话：010-67779337 E-mail:bjb@cnilas.org
技术支持：北京勤云科技发展有限公司
防诈骗提示！请勿点击不明链接或添加个人微信。编辑部所有邮箱后缀均为@cnilas.org
关闭