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Unlike other forms of regulated nonapoptotic cell death, ferroptosis is dependent on iron overload and characterized by the accretion of lipid peroxides[10, 11]

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In addition, experimental studies have shown that the elevation of GSH can inhibit the activation of hepatic stellate cells [33], which is a key driving factor for extracellular matrix deposition and fibrosis, thereby preventing the progression of liver fibrosis [34]

In healthy volunteers, iron loading under hypoxic conditions reduced or abolished the sensitivity of pulmonary vasculature to hypoxia, whereas iron chelation increased pulmonary artery systolic pressure and pulmonary vascular response to hypoxia [104]

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Notably, inhibition of either glycolysis or PPP (or conversely, promotion of mitochondrial respiration) reverses hypoxias capacity to maintain cellular stemness