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PUFAs evoke an inflammatory response of Gpx4 -deficient IECs To analyze the role of GPX4 in IECs, we first generated Gpx4 / small intestinal epithelial MODE-K cells by CRISPR Cas9 editing of exon 1 26 , which induced IEC death and thus prevented further studies (Supplementary Fig
Since the hallmark of SCD is chronic hemolysis with excess hemin producing significant levels of oxidative stress, we speculate that hemin may modulate TSS pathway function
doi: 10.3390/cells12060936 5
Sustained elevated glucose levels favor an imbalance between the availability of endothelial NO and the accumulation of ROS
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