c-Jun氨基端激酶信号通路调控急性呼吸窘迫综合征中重要炎症介质表达机制的研究进展
Research progress on the mechanisms of c-Jun N-terminal kinase signaling pathway in modulating the expression of important inflammatory mediators in acute respiratory distress syndrome
封岩 1胡蓉 2史家欣1
作者信息
- 1. 南京医科大学连云港临床医学院,江苏 连云港 222006
- 2. 南京医科大学附属连云港市第一人民医院,徐州医科大学附属连云港市第一人民医院呼吸与危重症医学科,江苏 连云港 222006
- 折叠
摘要
急性呼吸窘迫综合征(ARDS)是一种临床常见的危重症,其核心问题在于过度的炎症反应.c-Jun氨基端激酶(JNK)是促分裂原活化的蛋白质激酶(MAPK)家族最重要的成员之一,在调控细胞增殖、分化、凋亡、自噬及炎症等多个重要功能中发挥作用.JNK信号通路被过度激活时,会导致炎症反应的持续激活和炎症因子的过度生成,从而对机体造成严重损害.因此,明确JNK通过哪些信号通路参与炎症反应,对于控制ARDS的炎症进程和调节机体的免疫反应平衡具有重要意义.
Abstract
Acute respiratory distress syndrome(ARDS)is a common clinical critical illness with excessive inflammatory response at its core.c-Jun N-terminal kinase(JNK)is one of the most important members of the mitogen-activated protein kinase(MAPK)family,which plays a role in regulating several important functions including cell proliferation,differentiation,apoptosis,autophagy and inflammation.When the JNK signaling pathway is over-activated,it leads to sustained activation of inflammatory responses and overproduction of inflammatory factors,which can cause serious damage to the organism.Therefore,clarifying the signaling pathways through which JNK participates in the inflammatory response is important for controlling the inflammatory process in ARDS and regulating the balance of the body's immune response.
关键词
急性呼吸窘迫综合征/c-Jun氨基端激酶/炎症/炎症介质/信号通路Key words
acute respiratory distress syndrome/c-Jun N-terminal kinase/inflammation/inflammatory mediator/signaling pathway引用本文复制引用
基金项目
国家自然科学基金(81300052)
江苏省卫健委老年课题面上项目(LKM2022064)
连云港市卫健委资助项目(202016)
连云港市第一人民医院临床科研基金(LC10)
出版年
2024
NETL
NSTL
万方数据