The NOD-like receptor protein 3 (NLRP3) inflammasome is a central contributor to human acute and chronic liver disease, yet the molecular and cellular mechanisms by which its activation precipitates injury remain incompletely understood. Here, we present single cell transcriptomic profiling of livers from a global transgenic tamoxifen-inducible constitutively activated Nlrp3^A350V mutant mouse, and we investigate the changes in parenchymal and nonparenchymal liver cell gene expression that accompany inflammation and fibrosis.

中文翻译：

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NOD 样受体蛋白 3 激活会引起类似于人类 NASH 的自发炎症和纤维化


NOD 样受体蛋白 3 (NLRP3) 炎症小体是人类急性和慢性肝病的主要致病因素，但其激活导致损伤的分子和细胞机制仍不完全清楚。在这里，我们展示了来自全局转基因他莫昔芬诱导的组成型激活的Nlrp3 ^A350V突变小鼠肝脏的单细胞转录组分析，并研究了伴随炎症和纤维化的实质和非实质肝细胞基因表达的变化。