Association between NLRP3 inflammasome and periprocedural myocardial injury following elective PCI

BackgroundPeriprocedural myocardial injury (PMI) is a common complication of percutaneous coronary intervention (PCI) associated with poor prognosis. Inflammation has been demonstrated to exert crucial role in PMI. However, how the inflammation initiated or sustained PMI remains elusive.MethodsRNA-seq peripheral blood mononuclear cells (PBMCs) from 3 Non-PMI and 6 patients was performed subsequent bioinformatics analysis. RNA-seq results were verified patient cohort. We also established microembolization (CME) mice model mimic The activity caspase-1 PBMCs detected by flow cytometry. levels interleukin (IL)-1β, IL-18 cardiac troponin plasma measured enzyme-linked immunosorbent assay.ResultsWe identified total 901 differentially expressed genes (DEGs) between patients. These DEGs participated several inflammation-related processes. NOD-like receptor signaling pathway significantly enriched All key composed NLRP3 inflammasome, including NLRP3, PYCARD, CASP1 IL1B, upregulated activation inflammasome then increased PBMCs, elevated IL-1β Spearman analysis confirmed tight correlations activity, IL-1β, T level. In addition, enhanced CME mice.ConclusionsWe discovered that involved PMI, thus providing evidence supporting therapeutic value inflammasome-targeted strategies