Liao, Tingting; Xu, Xia; Ye, Xu; Yan, Jianying published the artcile< DJ-1 upregulates the Nrf2/GPX4 signal pathway to inhibit trophoblast ferroptosis in the pathogenesis of preeclampsia>, Product Details of C15H22N2O2, the main research area is DJ1 Nrf2 GPX4 signal trophoblast ferroptosis preeclampsia.
Ferroptosis is a newly discovered mode of cell death that involves disorders in iron metabolism and the accumulation of reactive oxygen species (ROS) in the plasma membrane. Preeclampsia (PE) is a gestational idiopathic disease that is characterized by hypertension and albuminuria, begins after 20 wk of pregnancy. DJ-1 is a prerequisite for activating and stabilizing Nrf2 to allow translocation to the nucleus to carry out further functions. Detecting the expression levels of DJ-1, the Nrf2/GPX4 signaling pathway and ferroptosis markers in placental tissues of pregnant women with and without PE. Analyzing the effects of the ferroptosis inducer (RSL3) and the inhibitor (Fer-1) on the mortality rate of BeWo cells and DJ-1+/+, DJ-1-/- BeWo cells. Ferroptosis markers (MDA concentration and morphol. of trophoblast cells) and DJ-1 and its downstream the Nrf2/GPX4 signaling pathway increased significantly in PE pathol. state. The expression levels of DJ-1 protein in the control group and the PE group were pos. correlated with the expression levels of Nrf2/GPX4 signaling pathway protein, and neg. correlated with the MDA concentration BeWo cells were sensitive to the ferroptosis inducer (RSL3) and the inhibitor (Fer-1). The high expression levels of DJ-1 in BeWo cells can resist ferroptosis by regulating the Nrf2/GPX4 signaling pathway. Ferroptosis is involved in the pathogenesis of PE. DJ-1 can mediate the trophoblast cells ferroptosis and play a protective role in the pathogenesis of preeclampsia by regulating the Nrf2/GPX4 signaling pathway.
Scientific Reports published new progress about Ferroptosis. 347174-05-4 belongs to class esters-buliding-blocks, and the molecular formula is C15H22N2O2, Product Details of C15H22N2O2.
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