No abstract

Ferroptosis is a name coined in 2012 for cell death driven by irondependent devastating lipid peroxidation (Shen et al., 2018). It is distinct from other cell death modes, including apoptosis and necrosis, in underlying mechanism, morphology and function in normal cell life (Yang & Stockwell, 2016). Ferroptotic cells appear with round cytoplasm and the normal nuclear size and chromatin density under light microscopy (Xie et al., 2016). From a mechanism perspective (Figure 1c), ferroptosis can be induced through inhibition of glutamate/cystine antiporter (system x − c ) by compounds like erastin, glutamate and sulfasalazine. Inactivation of glutathione peroxidase 4 (GPX4), which converts lipid hydroperoxides to non-toxic lipid alcohols (Stockwell et al., 2017), by compounds like RAS-selective lethal small molecule 3 (RSL3) or depletion of cells from reduced glutathione (GSH) (Yang & Stockwell, 2016) can also trigger ferroptosis. Moreover, inhibitors of the mevalonate pathway, such as statins, can initiate ferroptosis. They can impede with isopentenylation of selenocysteine-tRNA during the

No abstract