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Collectively, these metabolic alterations converge into a unified model of estrogen-deficiencydriven hepatic inflammation characterized by enhanced IDO1/TDO2KYN signaling, glycolytic reprogramming, phospholipid oxidation, TCA-cycle rewiring with itaconate accumulation, amino acid and purine pathway disruption, and redox imbalance through impaired PPP and taurine metabolism

Berning BA, Walker AK (2019) The pathobiology of TDP-43 C-terminal fragments in ALS and FTLD

ROS production increases during reperfusion, and factors like intracellular calcium overload can activate both extrinsic and intrinsic apoptotic pathways [14]