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中华临床医师杂志(电子版) ›› 2020, Vol. 14 ›› Issue (09) : 721 -724. doi: 10.3877/cma.j.issn.1674-0785.2020.09.011

所属专题: 文献

综述

野生型p53诱导的磷酸酶调节炎症和动脉粥样硬化研究进展
张颖怡1, 潘兵2, 王宏宇3,()   
  1. 1. 100144 北京大学首钢医院血管医学中心
    2. 100144 北京大学医学部血管健康研究中心;100191 北京大学心血管研究所
    3. 100144 北京大学首钢医院血管医学中心;100144 北京大学医学部血管健康研究中心
  • 收稿日期:2020-02-13 出版日期:2020-09-15
  • 通信作者: 王宏宇

Wild-type p53-induced phosphatase regulates immune inflammation and atherosclerosis

Yingyi Zhang1, Bing Pan2, Hongyu Wang3,()   

  1. 1. Department of Vascular Medicine, Peking University Shougang Hospital, Beijing 100144, China
    2. Vascular Health Research Center of Peking University Health Science Center, Beijing 100144, China; Institute of Cardiovascular Sciences, School of Basic Medical Sciences, Peking University Health Science Center, Beijing 100191, China
    3. Department of Vascular Medicine, Peking University Shougang Hospital, Beijing 100144, China; Vascular Health Research Center of Peking University Health Science Center, Beijing 100144, China
  • Received:2020-02-13 Published:2020-09-15
  • Corresponding author: Hongyu Wang
  • About author:
    Corresponding author: Wang Hongyu, Email:
引用本文:

张颖怡, 潘兵, 王宏宇. 野生型p53诱导的磷酸酶调节炎症和动脉粥样硬化研究进展[J/OL]. 中华临床医师杂志(电子版), 2020, 14(09): 721-724.

Yingyi Zhang, Bing Pan, Hongyu Wang. Wild-type p53-induced phosphatase regulates immune inflammation and atherosclerosis[J/OL]. Chinese Journal of Clinicians(Electronic Edition), 2020, 14(09): 721-724.

野生型p53诱导的磷酸酶(Wip1)是一种丝氨酸/苏氨酸磷酸酶,参与多种炎症相关疾病的免疫调节。最近研究发现,Wip1参与自噬、巨噬细胞迁移,平滑肌细胞增生,揭示Wip1参与了动脉粥样硬化(AS)过程。本文就Wip1与免疫炎症及AS关系的研究进展作一综述,希望为进一步探讨AS发生机制和AS相关疾病的治疗带来新思路。

Wild-type p53-induced phosphatase (Wip1) is a serine/threonine phosphatase that participates in the pathogenesis of inflammatory diseases. Recent studies have showed that Wip1 also plays a role in autophagy, macrophage migration, and vascular smooth muscle cell proliferation, which suggests that Wip1 also promotes the atherosclerosis (AS) process. In this paper, we review the relationship of Wip1 with immune inflammation and AS, in order to bring new ideas to the further exploration of targeted therapy for AS.

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