Ferroptotic stress enhances the accumulation of damage-associated inflammatory proximal tubular cell state, thereby promoting maladaptive renal repair and the AKI-to-CKD transition.

The neutral amino acid transporter SLC38A2 is an essential protective factor for renal medulla during urine concentration.

Ferroptosis is an evolutionary ancient process that is counterbalanced by distant peroxidases, GPx4 in mammals and tryparedoxin peroxidases in trypanosomes, and can be induced at distinct subcellular membranes depending on the individual cell type.

The accumulation of ferroptotic stress during tooth development has a critical effect on its morphogenesis.

Gut microbiota-derived gamma-aminobutyric acid is identified as a key metabolite that metformin protect from hepatic ischemia/reperfusion injury.

Hypobaric hypoxia exposure initiates splenic ferroptosis, reducing red pulp macrophages and exacerbating high-altitude polycythemia by impairing erythrophagocytosis and increasing red blood cell retention.

Mitochondrial functional and structural defects caused by PARL deficiency lead to arrested spermatogenesis and germ cell ferroptosis.

As worms age reduced glutathione together with increased ferrous iron increases frailty and leads to ferroptosis, which is amenable to therapeutic intervention.

Erastin and sorafenib inhibit system x_c^- and induce ER stress, suggesting these may be useful tools for probing the functions of system x_c^- and its role in inducing ER stress and ferroptosis.

IL4i1 is an amino acid oxidase expressed in the mammalian immune system and snake venoms, which control diametrically opposite cell protection versus cell death pathways, respectively.