Pyroptosis in platelets: Thrombocytopenia and inflammation

被引:7
作者
Su, Yang [1 ]
Zhang, Tiannan [1 ]
Qiao, Rui [1 ,2 ]
机构
[1] Peking Univ Third Hosp, Dept Lab Med, Beijing, Peoples R China
[2] Peking Univ Third Hosp, Dept Lab Med, Beijing 100191, Peoples R China
基金
中国国家自然科学基金;
关键词
caspase-1; GSDMD; inflammasome; NLRP3; platelets; pyroptosis; BRUTONS TYROSINE KINASE; ANTHRAX LETHAL TOXIN; NLRP3; INFLAMMASOME; IN-VITRO; MACROPHAGE APOPTOSIS; GASDERMIN D; CELL-DEATH; ACTIVATION; INTERLEUKIN-1; AGGREGATION;
D O I
10.1002/jcla.24852
中图分类号
R446 [实验室诊断]; R-33 [实验医学、医学实验];
学科分类号
1001 ;
摘要
ObjectiveThe purpose of this manuscript was to conclude the role of platelets in immune inflammation and discuss the complex mechanisms of pyroptosis in platelets as well as their related diseases. MethodsThis article reviewed the existing literature to see the development of pyroptosis in platelets. ResultsPlatelets have been shown to be capable of activating inflammasomes assembled from NOD-like receptor family pyrin domain containing 3 (NLRP3), apoptosis-associated speck-like protein containing a CARD (ASC) and caspase-1. Recently, they were also implicated in pyroptosis. Cleaved by caspase-1, N-terminal gasdermin D (N-GSDMD) could form pores in the cell membrane, inducing nonselective intracellular substance release. This programmed cell death induced thrombocytopenia and inflammatory cytokine release such as IL-1 beta and IL-18, promoting platelet aggregation, vaso-occlusion, endothelial permeability and cascaded inflammatory response. ConclusionPyroptosis in platelets contributes to thrombocytopenia and inflammation.
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页数:9
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