EPISODE · Aug 29, 2026 · 20 MIN
1510-湿地病毒诱发GSDME介导的肝细胞焦亡与脂肪代谢紊乱机制研究
from 聊聊Sci
这份研究揭示了湿地病毒（WELV）诱发致命性肝损伤的分子机制，指出该病毒通过激活GSDME蛋白介导的细胞焦亡，直接导致严重的肝脏脂肪变性。研究发现，病毒通过RIG-I信号通路同时触发细胞内源性和外源性凋亡级联反应，促使半胱天冬酶-3剪切GSDME，从而开启肝细胞焦亡进程。活化的GSDME能与脂肪酸合成酶（FASN）结合，阻止其降解并诱导脂质代谢重编程，最终引发肝脏脂质大量堆积。在小鼠模型中，敲除GSDME基因可完全抵御病毒感染带来的致死威胁。此外，使用临床批准的caspase抑制剂或FASN抑制剂（如奥利司他）能显著缓解病情并提高生存率。这些成果为应对这种新兴布尼亚病毒提供了关键的治疗靶点和潜在的药物方案。References:Wang C, Zheng X, Zhang Y, et al. Gasdermin E couples viral pyroptosis to lethal hepatic lipid accumulation[J]. Cell, 2026.前往小宇宙评论区与主播互动
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1510-湿地病毒诱发GSDME介导的肝细胞焦亡与脂肪代谢紊乱机制研究
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