Abstract
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.