血小板中的细胞焦亡：血小板减少症与炎症。
Pyroptosis in platelets: Thrombocytopenia and inflammation.
机构信息
Department of Laboratory Medicine, Peking University Third Hospital, Beijing, China.
出版信息
J Clin Lab Anal. 2023 Apr;37(4):e24852. doi: 10.1002/jcla.24852. Epub 2023 Feb 28.
OBJECTIVE
The 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.
METHODS
This article reviewed the existing literature to see the development of pyroptosis in platelets.
RESULTS
Platelets 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-1β and IL-18, promoting platelet aggregation, vaso-occlusion, endothelial permeability and cascaded inflammatory response.
CONCLUSION
Pyroptosis in platelets contributes to thrombocytopenia and inflammation.
目的
本文旨在总结血小板在免疫炎症中的作用，并探讨血小板细胞焦亡的复杂机制及其相关疾病。
方法
本文通过查阅现有文献，了解血小板细胞焦亡的发展情况。
结果
已有研究表明，血小板能够激活包含 NOD 样受体家族 pyrin 域包含 3（NLRP3）、凋亡相关斑点样蛋白包含 CARD（ASC）和半胱天冬酶-1 的炎症小体。最近，血小板细胞焦亡也被牵涉其中。天冬氨酸特异性半胱氨酸蛋白酶-1（caspase-1）切割后，N 端气 孔形成蛋白 D（N-GSDMD）可以在细胞膜上形成孔，诱导非选择性细胞内物质释放。这种程序性细胞死亡导致血小板减少和促炎细胞因子（如白细胞介素 1β 和白细胞介素 18）的释放，从而促进血小板聚集、血管阻塞、内皮通透性和级联炎症反应。
结论
血小板细胞焦亡导致血小板减少和炎症。
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