PI3K信号通路调控动脉粥样硬化发生发展的研究进展

doi:10.16352/j.issn.1001-6325.2022.09.1428

基础医学与临床 ›› 2022, Vol. 42 ›› Issue (9): 1428-1432.doi: 10.16352/j.issn.1001-6325.2022.09.1428

PI3K信号通路调控动脉粥样硬化发生发展的研究进展

刘珍竹¹, 李靖¹, 何丹^3*, 曲鹏^1,2*

1. 大连医科大学附属第二医院心内科,辽宁大连 116000;
2. 大连医科大学附属第二医院心脏及血管疾病研究所,辽宁大连 116000;
3. 北京大学医学部基础医学院生理学与病生理学系教育部分子心血管重点实验室,北京 100191

收稿日期:2021-02-09 修回日期:2021-07-17 出版日期:2022-09-05 发布日期:2022-09-02
通讯作者: dlhd820120@163.com;qupeng777@aliyun.com
基金资助:
国家自然科学基金(81670406, 82000415)

Research progress of PI3K signaling pathway regulating the pathogenesis of atherosclerosis

LIU Zhen-zhu¹, LI Jing¹, HE Dan^3*, QU Peng^1,2*

1. Department of Cardiology, the 2th Affiliated Hospital of Dalian Medical University, Dalian 116000;
2. Institute of Heart and Vascular Diseases, the 2th Affiliated Hospital of Dalian Medical University, Dalian 116000;
3. Department of Physiology and Pathophysiology, Key Laboratory of Molecular Cardiovascular Science, Ministry of Education, School of Basic Medical Sciences, Peking University, Beijing 100191, China

Received:2021-02-09 Revised:2021-07-17 Online:2022-09-05 Published:2022-09-02

摘要/Abstract

摘要： 磷脂酰肌醇3激酶(PI3K)信号通路参与动脉粥样硬化、肿瘤及免疫系统疾病的发生、发展。调节PI3K可以调控细胞凋亡、自噬、炎性反应等病理生理过程,为疾病的治疗提供了新思路。

关键词: 磷脂酰肌醇3激酶(PI3K), 动脉粥样硬化, 免疫炎性反应

Abstract: Phosphatidylinositol 3-kinase(PI3K) signaling pathway is involved in the occurrence and development of atherosclerosis, tumor and immune system diseases. Regulation of PI3K can regulate apoptosis, autophagy, inflammatory response and other pathophysiological processes, which provides a new idea for the treatment of diseases.

Key words: phosphatidylinositol 3-kinase(PI3K), atherosclerosis, immune inflammation

中图分类号:

R364.5

刘珍竹, 李靖, 何丹, 曲鹏. PI3K信号通路调控动脉粥样硬化发生发展的研究进展[J]. 基础医学与临床, 2022, 42(9): 1428-1432.

LIU Zhen-zhu, LI Jing, HE Dan, QU Peng. Research progress of PI3K signaling pathway regulating the pathogenesis of atherosclerosis[J]. Basic & Clinical Medicine, 2022, 42(9): 1428-1432.

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PI3K信号通路调控动脉粥样硬化发生发展的研究进展

Research progress of PI3K signaling pathway regulating the pathogenesis of atherosclerosis

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