引言
铁死亡(Ferroptosis)是区别于细胞凋亡、坏死、自噬的一种新型调节性的细胞死亡方式【1】,由铁依赖的脂质过氧化物积累所导致,铁死亡的诱发在许多疾病(如缺血再灌注心肌损伤、神经退行性病变、自身免疫性以及传染性疾病)中起关键致病作用【2,3】,同时也是临床中治疗肿瘤的新型手段【4,5】。诱发细胞铁死亡的主要因素包括ROS(•OH)、含有多不饱和脂肪酸的磷脂(PUFA-PL)和Fe2+,因而铁死亡严格受到氧化还原稳态、铁代谢和脂代谢的调控。近年来,糖代谢和氨基酸代谢对铁死亡的调控作用也日渐凸显,但具体精细的调节机制很大程度上仍然未知。
2024年10月17日,东北师范大学分子表观遗传学教育部重点实验室魏民/王杨团队与巴雪青团队合作在Nature Communications上发表了题为Methionine-SAM metabolism-dependent ubiquinone synthesis is crucial for ROS accumulation in ferroptosis induction的研究论文,系统地报道了甲硫氨酸衍生的S-腺苷甲硫氨酸(S-adenosylmethionine, SAM)促进电子载体泛醌(Ubiquinone, UQ)的合成及线粒体ROS的产生,是细胞发生铁死亡的必要条件。

参考文献
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排版|探索君
来源|BioArt
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