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Inhibition of GPR109A can be accomplished through the Gln metabolism/ER stress/GPR109A axis

Consistent with this, pharmacological inhibition of coagulation by heparin and genetic approaches (mice deficient in either tissue factor or PAR-1) attenuate APAP hepatotoxicity at an early stage (6 h) [33]

Meanwhile, changes in mitochondrial function may also be due to ROS caused by iron elevation during ferroptosis related to mitophagy

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