留言板

尊敬的读者、作者、审稿人, 关于本刊的投稿、审稿、编辑和出版的任何问题, 您可以本页添加留言。我们将尽快给您答复。谢谢您的支持!

姓名
邮箱
手机号码
标题
留言内容
验证码
x

氧化应激与自噬在动脉粥样硬化发生发展中的研究进展

薛万华 杨婷

薛万华, 杨婷. 氧化应激与自噬在动脉粥样硬化发生发展中的研究进展[J]. 分子影像学杂志, 2019, 42(1): 95-98. doi: 10.12122/j.issn.1674-4500.2019.01.22
引用本文: 薛万华, 杨婷. 氧化应激与自噬在动脉粥样硬化发生发展中的研究进展[J]. 分子影像学杂志, 2019, 42(1): 95-98. doi: 10.12122/j.issn.1674-4500.2019.01.22
Wanhua XUE, Ting YANG. Recent advances in atherosclerosis of oxidative stress and autophagy[J]. Journal of Molecular Imaging, 2019, 42(1): 95-98. doi: 10.12122/j.issn.1674-4500.2019.01.22
Citation: Wanhua XUE, Ting YANG. Recent advances in atherosclerosis of oxidative stress and autophagy[J]. Journal of Molecular Imaging, 2019, 42(1): 95-98. doi: 10.12122/j.issn.1674-4500.2019.01.22

氧化应激与自噬在动脉粥样硬化发生发展中的研究进展

doi: 10.12122/j.issn.1674-4500.2019.01.22
详细信息
    作者简介:

    薛万华:薜万华,主任技师,E-mail: 543328707@qq.com

    通讯作者:

    杨 婷,硕士,检验技师,E-mail: yangting8912@126.com

Recent advances in atherosclerosis of oxidative stress and autophagy

  • 摘要: 动脉粥样硬化是一种以大中动脉血管壁脂质堆积和慢性炎症反应为特点的疾病,其发生过程十分复杂,目前对其发生发展机制的研究已形成多种学说,氧化应激学说是其重要组成部分,当机体产生的高活性氧自由基在粥样硬化斑块处堆积时,会造成血管损伤,促进动脉粥样硬化的发生。自噬是细胞清除胞内错误折叠的蛋白质或受损细胞器,维持内环境稳态的重要方式,研究证明其在动脉粥样硬化过程中也起着重要作用。本文主要对近年来氧化应激和自噬在动脉粥样硬化发生发展中的研究新进展做一综述,为进一步阐明动脉粥样硬化的发生机制和未来进行针对性治疗提供理论基础。

     

  • [1] Li TB, Zhang JJ, Liu B, et al. Dysfunction of endothelial progenitor cells in hyperlipidemic rats involves the increase of NADPH oxidase derived reactive oxygen species production[J]. Can J Physiol Pharmacol, 2017, 95(5): 474-80 doi: 10.1139/cjpp-2016-0142
    [2] Forstermann U, Xia N, Li H. Roles of Vascular Oxidative Stress and Nitric Oxide in the Pathogenesis of Atherosclerosis[J]. Circ Res, 2017, 120(4): 713-5 doi: 10.1161/CIRCRESAHA.116.309326
    [3] Bryk D, Olejarz W, Zapolska-Downar D. The role of oxidative stress and NADPH oxidase in the pathogenesis of atherosclerosis[J]. Postepy Hig Med Dosw (Online), 2017, 71(1): 57-68 doi: 10.5604/00325449
    [4] Drummond GR and Sobey CG. Endothelial NADPH oxidases: which NOX to target in vascular disease[J]. Trends Endocrinol Metab, 2014, 25(9): 452-63 doi: 10.1016/j.tem.2014.06.012
    [5] Di Marco E, Gray SP, Chew P, et al. Pharmacological inhibition of NOX reduces atherosclerotic lesions, vascular ROS and immune-inflammatory responses in diabetic Apoe(-/-) mice[J]. Diabetologia, 2014, 57(3): 633-42 doi: 10.1007/s00125-013-3118-3
    [6] Sobey CG, Judkins CP, Rivera J, et al. NOX1 deficiency in apolipoprotein E-knockout mice is associated with elevated plasma lipids and enhanced atherosclerosis[J]. Free Radic Res, 2015, 49(2): 186-98 doi: 10.3109/10715762.2014.992893
    [7] Gray SP, Jha JC, Kennedy K, et al. Combined NOX1/4 inhibition with GKT137831 in mice provides dose-dependent reno- and atheroprotection even in established micro- and macrovascular disease[J]. Diabetologia, 2017, 60(5): 927-37 doi: 10.1007/s00125-017-4215-5
    [8] Violi F, Carnevale R, Loffredo L, et al. NADPH Oxidase-2 and atherothrombosis: insight from chronic granulomatous disease[J]. Arterioscler Thromb Vasc Biol, 2017, 37(2): 218-25 doi: 10.1161/ATVBAHA.116.308351
    [9] Lozhkin A, Vendrov AE, Pan H, et al. NADPH oxidase 4 regulates vascular inflammation in aging and atherosclerosis[J]. J Mol Cell Cardiol, 2017, 102(1): 10-21
    [10] Schurmann C, Rezende F, Kruse C, et al. The NADPH oxidase Nox4 has anti-atherosclerotic functions[J]. Eur Heart J, 2015, 36(48): 3447-56 doi: 10.1093/eurheartj/ehv460
    [11] Gray SP, Di Marco E, Kennedy K, et al. Reactive oxygen species can provide atheroprotection via NOX4-dependent inhibition of inflammation and vascular remodeling[J]. Arterioscler Thromb Vasc Biol, 2016, 36(2): 295-307 doi: 10.1161/ATVBAHA.115.307012
    [12] Manea A, Manea SA, Florea IC, et al. Positive regulation of NADPH oxidase 5 by proinflammatory-related mechanisms in human aortic smooth muscle cells[J]. Free Radic Biol Med, 2012, 52(9): 1497-507 doi: 10.1016/j.freeradbiomed.2012.02.018
    [13] Guo FX, Hu YW, Zheng L, et al. Shear stress in autophagy and its possible mechanisms in the process of atherosclerosis[J]. DNA Cell Biol, 2017, 36(5): 335-46 doi: 10.1089/dna.2017.3649
    [14] Yoon WS, Yeom MY, Kang ES, et al. Memantine induces NMDAR1-mediated autophagic cell death in malignant glioma cells[J]. J Korean Neurosurg Soc, 2017, 60(2): 130-7 doi: 10.3340/jkns.2016.0101.006
    [15] Ding Z, Liu S, Wang X, et al. Oxidant stress in mitochondrial DNA damage, autophagy and inflammation in atherosclerosis[J]. Sci Rep, 2013, 3(10): 1077-82
    [16] Liao X, Sluimer JC, Wang Y, et al. Macrophage autophagy plays a protective role in advanced atherosclerosis[J]. Cell Metab, 2012, 15(4): 545-53 doi: 10.1016/j.cmet.2012.01.022
    [17] Martinet W, Schrijvers DM, Timmermans JP, et al. Interactions between cell death induced by statins and 7-ketocholesterol in rabbit aorta smooth muscle cells[J]. Br J Pharmacol, 2008, 154(6): 1236-46 doi: 10.1038/bjp.2008.181
    [18] Mollace V, Gliozzi M, Musolino V, et al. Oxidized LDL attenuates protective autophagy and induces apoptotic cell death of endothelial cells: Role of oxidative stress and LOX-1 receptor expression[J]. Int J Cardiol, 2015, 184(2): 152-8
    [19] Zhang M, Zhu H, Ding Y, et al. AMP-activated protein kinase alpha1 promotes atherogenesis by increasing monocyte-to-macrophage differentiation[J]. J Biol Chem, 2017, 45(4): 447-51
    [20] Zhai C, Cheng J, Mujahid H, et al. Selective inhibition of PI3K/Akt/mTOR signaling pathway regulates autophagy of macrophage and vulnerability of atherosclerotic plaque[J]. PLoS One, 2014, 9(3): e90563-7 doi: 10.1371/journal.pone.0090563
    [21] Li R, Ji Z, Qin H, et al. Interference in autophagosome fusion by rare earth nanoparticles disrupts autophagic flux and regulation of an interleukin-1beta producing inflammasome[J]. ACS Nano, 2014, 8(10): 10280-92 doi: 10.1021/nn505002w
    [22] Li L, Tan J, Miao Y, et al. ROS and autophagy: interactions and molecular regulatory mechanisms[J]. Cell Mol Neurobiol, 2015, 35(5): 615-21 doi: 10.1007/s10571-015-0166-x
    [23] Ding Z, Wang X, Schnackenberg L, et al. Regulation of autophagy and apoptosis in response to ox-LDL in vascular smooth muscle cells, and the modulatory effects of the microRNA hsa-let-7 g[J]. Int J Cardiol, 2013, 168(2): 1378-85 doi: 10.1016/j.ijcard.2012.12.045
    [24] Ding Z, Liu S, Wang X, et al. LOX-1, oxidant stress, mtDNA damage, autophagy, and immune response in atherosclerosis[J]. Can J Physiol Pharmacol, 2014, 92(7): 524-30 doi: 10.1139/cjpp-2013-0420
    [25] Martinet W, de Meyer GR. Autophagy in atherosclerosis: a cell survival and death phenomenon with therapeutic potential[J]. Circ Res, 2009, 104(3): 304-17 doi: 10.1161/CIRCRESAHA.108.188318
    [26] Van Heerebeek L, Meischl C, Stooker W, et al. NADPH oxidase(s): new source(s) of reactive oxygen species in the vascular system[J]. J Clin Pathol, 2002, 55(8): 561-8 doi: 10.1136/jcp.55.8.561
    [27] Kaushik S, Cuervo AM. Autophagy as a cell-repair mechanism: activation of chaperone-mediated autophagy during oxidative stress[J]. Mol Aspects Med, 2006, 27(5): 444-54
    [28] Oh SH, Kim YS, Lim SC, et al. Dihydrocapsaicin (DHC), a saturated structural analog of capsaicin, induces autophagy in human cancer cells in a catalase-regulated manner[J]. Autophagy, 2008, 4(8): 1009-19 doi: 10.4161/auto.6886
    [29] Jain A, Lamark T, Sjottem E, et al. p62/SQSTM1 is a target gene for transcription factor NRF2 and creates a positive feedback loop by inducing antioxidant response element-driven gene transcription[J]. J Biol Chem, 2010, 285(29): 22576-91 doi: 10.1074/jbc.M110.118976
    [30] Li GH, Lin XL, Zhang H, et al. Ox-Lp(a) transiently induces HUVEC autophagy via an ROS-dependent PAPR-1-LKB1-AMPK-mTOR pathway[J]. Atherosclerosis, 2015, 243(1): 223-35 doi: 10.1016/j.atherosclerosis.2015.09.020
  • 加载中
计量
  • 文章访问数:  790
  • HTML全文浏览量:  381
  • PDF下载量:  25
  • 被引次数: 0
出版历程
  • 收稿日期:  2018-08-13
  • 刊出日期:  2019-01-01

目录

    /

    返回文章
    返回