氧化应激与自噬在动脉粥样硬化发生发展中的研究进展

被引：20

作者：

薛万华

杨婷

机构：

[1] 德州市人民医院检验科

来源：

分子影像学杂志 | 2019年 / 42卷 / 01期

关键词：

氧化应激; 自噬; 动脉粥样硬化;

D O I：

暂无

中图分类号：

R543.5 [动脉疾病];

学科分类号：

100201 [内科学];

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。

引用

页码：95 / 98

页数：4

共 15 条

[1]

AMP-activated protein kinase α1 promotes atherogenesis by increasing monocyte-to-macrophage differentiation [J].

Zhang, Miao ;

Zhu, Huaiping ;

Ding, Ye ;

Liu, Zhaoyu ;

Cai, Zhejun ;

Zou, Ming-Hui .

JOURNAL OF BIOLOGICAL CHEMISTRY, 2017, 292 (19) :7888-7903

[2]

Combined NOX1/4 inhibition with GKT137831 in mice provides dose-dependent reno- and atheroprotection even in established micro- and macrovascular disease [J].

Gray, Stephen P. ;

Jha, Jay C. ;

Kennedy, Kit ;

van Bommel, Erik ;

Chew, Phyllis ;

Szyndralewiez, Cedric ;

Touyz, Rhian M. ;

Schmidt, Harald H. H. W. ;

Cooper, Mark E. ;

Jandeleit-Dahm, Karin A. M. .

DIABETOLOGIA, 2017, 60 (05) :927-937

[3]

NADPH oxidase 4 regulates vascular inflammation in aging and atherosclerosis.[J].Andrey Lozhkin;Aleksandr E. Vendrov;Hua Pan;Samuel A. Wickline;Nageswara R. Madamanchi;Marschall S. Runge.Journal of Molecular and Cellular Cardiology.2017,

[4]

Ox-Lp(a) transiently induces HUVEC autophagy via an ROS-dependent PAPR-1-LKB1–AMPK–mTOR pathway.[J].Guo-hua Li;Xiao-long Lin;Hai Zhang;Shuang Li;Xing-lan He;Kai Zhang;Juan Peng;Ya-ling Tang;Jun-fa Zeng;Yue Zhao;Xiao-feng Ma;Jian-jun Lei;Ren Wang;Dang-heng Wei;Zhi-Sheng Jiang;Zuo Wang.Atherosclerosis.2015, 1

[5]

Oxidized LDL attenuates protective autophagy and induces apoptotic cell death of endothelial cells: Role of oxidative stress and LOX-1 receptor expression.[J].Vincenzo Mollace;Micaela Gliozzi;Vincenzo Musolino;Cristina Carresi;Saverio Muscoli;Rocco Mollace;Annamaria Tavernese;Santo Gratteri;Ernesto Palma;Chiara Morabito;Cristiana Vitale;Carolina Muscoli;Massimo Fini;Francesco Romeo.International Journal of Cardiology.2015,

[6]

NOX1 deficiency in apolipoprotein E-knockout mice is associated with elevated plasma lipids and enhanced atherosclerosis [J].

Sobey, C. G. ;

Judkins, C. P. ;

Rivera, J. ;

Lewis, C. V. ;

Diep, H. ;

Lee, H. W. ;

Kemp-Harper, B. K. ;

Broughton, B. R. S. ;

Selemidis, S. ;

Gaspari, T. A. ;

Samuel, C. S. ;

Drummond, G. R. .

FREE RADICAL RESEARCH, 2015, 49 (02) :186-198

[7]

Endothelial NADPH oxidases: which NOX to target in vascular disease? [J].

Drummond, Grant R. ;

Sobey, Christopher G. .

TRENDS IN ENDOCRINOLOGY AND METABOLISM, 2014, 25 (09) :452-463

[8]

Pharmacological inhibition of NOX reduces atherosclerotic lesions; vascular ROS and immune–inflammatory responses in diabetic Apoe ?/? mice.[J].E. Marco;S. P. Gray;P. Chew;C. Koulis;A. Ziegler;C. Szyndralewiez;R. M. Touyz;H. H. H. W. Schmidt;M. E. Cooper;R. Slattery;K. A. Jandeleit-Dahm.Diabetologia.2014, 3

[9]

Macrophage Autophagy Plays a Protective Role in Advanced Atherosclerosis [J].