1510-GasderminE-Viral Pyroptosis to Lethal Hepatic Steatosis

The research study examines the pathogenic mechanisms of the emerging tick-borne wetland virus (WELV), identifying it as a significant cause of lethal liver dysfunction. The authors demonstrate that infection triggers GSDME-dependent pyroptosis, a form of inflammatory cell death, through the activation of both intrinsic and extrinsic apoptotic pathways. This process is initiated when viral RNA is recognized by the RIG-I sensor, which subsequently drives a pyroptosis-metabolism axis. A key finding reveals that GSDME physically stabilizes fatty acid synthase (FASN), preventing its degradation and leading to severe hepatic steatosis and lipid accumulation. To counter this, the study identifies that the viral nucleoprotein can act as a sequestrator of caspase-3 to temporarily mitigate cell death. Finally, the researchers show that targeting this axis with caspase or FASN inhibitors significantly improves survival rates in animal models, offering a promising therapeutic strategy for treating the infection.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