摘要
细胞焦亡是由gasdermin家族蛋白D(gasdermin D,GSDMD)介导的一种新型程序性细胞死亡方式,表现为早期细胞凋亡样染色质凝结和DNA断裂,之后形成细胞膜孔,细胞肿胀,膜破裂,导致细胞内容物和促炎介质的释放。细胞焦亡途径主要包括依赖含半胱氨酸的天冬氨酸蛋白水解酶1(cysteinyl aspartate specific proteinase-1,caspase-1)的经典途径和依赖caspase-4/caspase-5/caspase-11的非经典途径。细胞焦亡的主要特点是Nod样受体蛋白3(nod-like receptor protein 3,NLRP3)炎性小体活化,caspase-1激活,细胞膜孔形成,白细胞介素(interleukin,IL)-1β和IL-18释放,从而放大炎症级联反应。NLRP3炎性小体活化与高血压、糖尿病、高脂血症及肥胖等心血管危险因素有关,是心血管炎症的重要触发和内源性调节因子。本文主要就细胞焦亡在心血管疾病中的相关研究进展进行综述。
Pyroptosis is a new type of programmed cell death mediated by gasdermin D(GSDMD)protein.It is characterized by early apoptosis like chromatin condensation and DNA fragmentation,followed by the formation of cell membrane pores,cell swelling and membrane rupture,resulting in the release of cell contents and pro-inflammatory mediators.The pyroptotic pathway mainly includes canonical pathway dependent on caspase-1 and noncanonical pathway dependent on caspase-4/caspase-5/caspase-11.The main characteristics of pyroptosis are the activation of inflammatory corpuscles of nod-like receptor protein 3(NLRP3),the activation of caspase-1,the formation of cell membrane pore,and the release of interleukin-1βand IL-18,thus amplifying the inflammatory cascade.Recent studies have found that NLRP3 inflammasome activation is associated with cardiovascular risk factors such as hypertension,diabetes,hyperlipidemia and obesity,and is an important trigger and endogenous regulator of cardiovascular inflammation.In this paper,we reviewed the research progress of the role of pyroptosis in cardiovascular diseases.
作者
王文丽
孙思雨
杨瑞瑞
贺忠梅
WANG Wenli;SUN Siyu;YANG Ruirui;HE Zhongmei(Department of Physiology,Shanxi Medical University,Key Laboratory of Cellular Physiology,Ministry of Education,Taiyuan 030000,China)
出处
《生命的化学》
CAS
2021年第4期741-747,共7页
Chemistry of Life
基金
山西省回国留学人员科研项目(2020-078)
山西省自然科学基金项目(201601D011115)。
