Mitochondrial GRIM19 Loss Induces Liver Fibrosis through NLRP3/IL33 Activation via Reactive Oxygen Species/NF-кB Signaling

作者：Xiaohui Xu, Jinmei Feng, Xin Wang, Xin Zeng, Ying Luo, Xinyu He, Meihua Yang, Tiewei Lv, Zijuan Feng, Liming Bao, Li Zhao, Daochao Huang, Yi Huang · 发表于：Journal of Clinical and Translational Hepatology · 年份：2024 · DOI：10.14218/jcth.2023.00562 · 被引用次数：10 · 研究领域：interferon and immune responses、Retinoids in leukemia and cellular processes、Hepatocellular Carcinoma Treatment and Prognosis

Background and Aims: Hepatic fibrosis (HF) is a critical step in the progression of hepatocellular carcinoma (HCC). Gene associated with retinoid-IFN-induced mortality 19 (GRIM19), an essential component of mitochondrial respiratory chain complex I, is frequently attenuated in various human cancers, including HCC. Here, we aimed to investigate the potential relationship and underlying mechanism between GRIM19 loss and HF pathogenesis. Methods: . We performed flow cytometry, immunofluorescence, immunohistochemistry, western blotting, and pharmacological intervention to uncover the potential mechanisms underlying GRIM19 loss-induced HF. Results: . Conclusions: The mitochondrial GRIM19 loss facilitates liver fibrosis through NLRP3/IL33 activation via ROS/NF-кB signaling, providing potential therapeutic approaches for earlier HF prevention.