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5 个月
PROM2通过激活NLRP3炎症小体和肝细胞焦亡加剧四氯化碳诱导的肝纤维化
本研究揭示了PROM2在肝纤维化中的关键作用。研究人员通过转录组学分析和体内模型证实PROM2通过激活NLRP3炎症小体通路和促进上皮-间质转化(EMT)加剧肝纤维化进程。研究发现PROM2缺失可显著减轻肝脏炎症和纤维化,而NLRP3基因敲除可消除PROM2的促纤维化效应,表明 ...
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