Phospholipase iPLA2β acts as a guardian against ferroptosis  

作　　者：Chao Mao Guang Lei Li Zhuang Boyi Gan 

机构地区：[1]Department of Experimental Radiation Oncology,The University of Texas MD Anderson Cancer Center,Houston,TX 77030,USA [2]The University of Texas MD Anderson UTHealth Graduate School of Biomedical Sciences,Houston,TX 77030,USA

出　　处：《Cancer Communications》2021年第11期1082-1085,共4页癌症通讯（英文）

基　　金：Research in the authors’lab has been supported by The University of Texas MD Anderson Cancer Center,National Institutes of Health grants R01CA181196,R01CA244144,and R01CA247992(to BG);by Cancer Center Sup-port(Core)Grant P30 CA016672 from the National Cancer Institute(to The University of Texas MD Anderson Cancer Center).

摘　　要：Ferroptosis,a form of iron-dependent regulated cell death caused by excessive accumulation of lipid hydroperoxides,has been associated with various pathological conditions and diseases[1].Excessive ferroptosis has been causally associated with acute kidney injury,cardiovascular,neurodegenerative and hepatic diseases,whereas impaired ferroptosis in premalignant cells has been shown to contribute to tumor development[2,3].To escape from ferroptotic cell death,cells have been equipped with several antioxidant defense systems against lipid peroxidation(Figure 1).Glutathione peroxidase 4(GPX4)suppresses ferroptosis by converting lipid hydroperoxides into non-toxic lipid alcohols at the expense of its cofactor glutathione(GSH)[4].Ferroptosis suppressor protein-1(FSP1,also known as AIFM2),a NAD(P)H-dependent oxidoreductase located on the plasma membrane,catalyzes the reduction of ubiquinone to ubiquinol,a radical trapping antioxidant that suppresses ferroptosis independent of the GSH-GPX4 axis[5,6].In addition,dihydroorotate dehydrogenase(DHODH),an enzyme involved in the de novo pyrimidine biosynthesis pathway,inhibits ferroptosis by reducing ubiquinone to ubiquinol in the inner mitochondrial membrane[7].

关 键 词：FIGURE equipped ALCOHOLS 

分 类 号：O62[理学—有机化学]