Table 1.

Ferroptosis in pathological conditions

Diffuse large B cell lymphoma (DLBCL)	Intrinsically more sensitive to ferroptosis inducers [16] Dependent on cysteine/cystine import system (system xc−) due to defective transsulfuration pathway in DLBCL [58, 59]
Chromophobe renal cell carcinoma	Intense iron staining in the tumor tissue (iron rich enviroment) [61]
Acute kidney failure by rhadomyolysis	Ferrostatin-1 prevented cell death in an ex vivo model of rhabdomyolysis-induced acute kidney injury [40] Myolysis releases myoglobin and heme iron causing ROS generation and acute kidney injury [38]
Acute kidney failure by ischemia-reperfusion injury	16–86, a third generation ferrostatin, protected mice from acute renal failure due to ischemia-reperfusion injury [41]
Huntington's disease	Ferrostatin-1 prevented cell death in an organotypic slice culture model of Huntington's disease [40]
Periventricular Leukomalacia (PVL)	Lipid peroxidation products detected in 33 human autopsy brains with PVL [47] Premature oligodendrocytes (OLs) were more sensitive to GSH depletion-induced cell death [49] Ferrostatin-1 prevented cell death in an OL culture model of PVL [40]
SBP2 deficiency syndrome	Mutation in SBP2 prevents translation of selenoproteins including GPX4 [53] Fibroblasts from patients showed increased basal level of lipid-ROS [53]
Sedaghatian-type spondylometaphyseal dysplasia	Loss of function mutation in GPX4 is associated with neonatal lethality of affected children [36]