意大利贵宾

Sui等^[2]研究发明在大鼠肝纤维化模子中，，异甘草酸镁可诱导 HO-1上调，，增进铁和脂质过氧化物的积累，，从而增进HSC铁殒命的爆发；；；而通过铁殒命抑制剂ferrostatin-1或默然HO-1则消除了异甘草酸镁的抗纤维化作用。。
。。。锌指卵白36(ZFP36 ring finger protein 36，，ZFP36/TTP)和胚胎致死性异常视觉样卵白1(ELAV like RNA binding protein 1，，ELAVL1/HuR) 在调控HSC铁殒命中施展主要作用，，下调 ZFP36和上调ELAVL1可以增进索拉非尼(sorafenib)/erastin介导的HSC铁殒命，，减轻小鼠肝纤维化，，进一步机制研究发明ZFP36/ELAVL1可能与下游靶基因连系，，影响其mRNA稳固性，，从而调控HSC中储铁卵白自噬，，释放出铁离子，，继而通过芬顿反应爆发大宗ROS，，增进HSC铁殒命^[3,4] 。。
。。。

Zhang等^[5]研究发明接纳CRISPR/cas9介导的BRD7敲除可镌汰HSC铁殒命，，而特异性BRD7质粒介导的BRD7过表达可增进HSC铁殒命，，进一步研究发明BRD7表达升高可通过直接与P53 N-最后转激活域连系增进P53线粒体转位，，从而与下游SLC25A28相互作用形成复合物来介导铁殒命的爆发。。
。。。研究者发明小鼠肝细胞特异性敲除Trf体现为肝脏非转铁卵白连系铁蓄积，，加重高铁饮食介导的肝纤维化，，而同时特异性敲除小鼠肝细胞Trf和溶质载体家族39成员14(solute carrier family 39 member 14，，SLC39A14) 可显著镌汰肝脏铁的积累，，改善了高铁膳食或四氯化碳注射介导的肝纤维化，，这些数据批注肝脏转铁卵白在维持肝功效方面施展；；；ぷ饔茫，为预防铁过载诱导的肝纤维化提供了一个潜在治疗靶点^[6]。。
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现在研究以为，，铁殒命的最终执行机制是由于过量的脂质过氧化物累积引起质膜损伤，，造成细胞铁殒命的爆发。。
。。。Sun等^[7]研究报道，，默然P62表达会增添erastin/sorafenib诱导的肝细胞癌(hepatocellular carcinoma，，HCC) 细胞铁殒命。。
。。。别的，，在HCC细胞移植瘤小鼠模子以及细胞实验中发明，，核因子E2-相关因子2(nuclear factor erythroid 2-related factor 2，，Nrf2) 敲低也体现出增强erastin/sorafenib抗HCC的作用。。
。。。这些效果批注，，P62-Kelch样ECH关联卵白1(Kelch-like ECH-associating protein 1，，Keap1)-Nrf2信号通路可能在铁殒命中施展主要作用。。
。。。因此，，Nrf2可能是加入铁殒命及未来治疗多种肝病的主要靶点。。
。。。

 作为生命科学及医学领域的卵白抗体供应商，，ELK biotechnology可为铁殒命相关研究提供高品质的试剂，，这里将铁殒命部分产品列出来以便各人参考，，详情见下表：

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