ライフサイエンスコーパス: ferroptosis

1 nction of a selenoperoxidase, GPX4, leads to ferroptosis.

2 ulates reactive oxygen species (ROS)-induced ferroptosis.

3 urons and dynamic glutathione changes during ferroptosis.

4 not be compensated, leading to cell death by ferroptosis.

5 D-PUFA) prevented PUFA oxidation and blocked ferroptosis.

6 yunsaturated fatty acids and is required for ferroptosis.

7 expression partially abrogates p53-mediated ferroptosis.

8 lutamine, were identified as the inducers of ferroptosis.

9 ner, which was subsequently determined to be ferroptosis.

10 ion of cystine metabolism, ROS responses and ferroptosis.

11 expression of HSPB1 inhibits erastin-induced ferroptosis.

12 c (-) function and can trigger ER stress and ferroptosis.

13 e particularly susceptible to GPX4-regulated ferroptosis.

14 form of nonapoptotic cell death that we term ferroptosis.

15 Increases in lipid peroxidation can cause ferroptosis, a form of cell death triggered by inhibitio

16 Ferrostatin-1 (Fer-1) inhibits ferroptosis, a form of regulated, oxidative, nonapoptoti

17 pid-peroxidase pathway that protects against ferroptosis, a non-apoptotic form of cell death induced

18 tive damage to lipids, is a key inhibitor of ferroptosis, a non-apoptotic form of cell death involvin

19 ibits cystine uptake and sensitizes cells to ferroptosis, a non-apoptotic form of cell death, by repr

20 bition of glutathione biosynthesis, triggers ferroptosis, a non-apoptotic form of cell death.

21 g how damage to cell membranes occurs during ferroptosis, an iron-dependent form of regulated cell de

22 and its overexpression inhibits ROS-induced ferroptosis and abrogates p53(3KR)-mediated tumour growt

23 iscovery of multiple molecular components of ferroptosis and its intimate interplay with cellular met

24 We explored the relative contributions of ferroptosis and necroptosis to folic acid (FA)-induced A

25 a PHKG2-dependent iron pool is necessary for ferroptosis and that the covalent inhibition of the cata

26 osis, pyroptosis, pyronecrosis, necroptosis, ferroptosis, and parthanatos were excluded as modes of o

27 However, the mechanisms of ferroptosis are not well defined.

28 gents that induce iron-dependent cell death (ferroptosis) as well as iron chelators, and thus creates

29 lacking alpha6beta4 is sufficient to trigger ferroptosis because GPX4 is suppressed.

30 uire an inducer, such as erastin, to undergo ferroptosis because they sustain GPX4 expression, despit

31 concomitantly underwent cell death driven by ferroptosis but not necroptosis.

32 1 phosphorylation confers protection against ferroptosis by reducing iron-mediated production of lipi

33 These data demonstrate that ferroptosis can be targeted by ultrasmall silica nanopar

34 Ferroptosis can be triggered by depleting the cell of th

35 f glutaminolysis, the essential component of ferroptosis, can reduce heart injury triggered by ischem

36 related non-apoptotic pathways suggest that ferroptosis could be an adaptive process, albeit one reg

37 ntation with vitamin E, another inhibitor of ferroptosis, delayed the onset of paralysis and death in

38 In contrast, iron-dependent ferroptosis directly causes synchronized necrosis of ren

39 With respect to the immunogenicity of ferroptosis, Fer-1 prevented the upregulation of IL-33,

40 Ferroptosis has been implicated in the pathological cell

41 Although ferroptosis has been suggested to involve accumulation o

42 Ferroptosis has emerged as a new form of regulated necro

43 This causal link between alpha6beta4 and ferroptosis has implications for cancer biology and ther

44 his Primer reviews the mechanisms underlying ferroptosis, highlights connections to other areas of bi

45 sequence, ARF expression sensitizes cells to ferroptosis in a p53-independent manner while ARF deplet

46 ss in Arabidopsis thaliana The similarity of ferroptosis in animal cells and ferroptosis-like death i

47 ecule ferrostatin-1 as a potent inhibitor of ferroptosis in cancer cells and glutamate-induced cell d

48 dings suggest new strategies for controlling ferroptosis in diverse contexts.

49 n tension and protects cells from undergoing ferroptosis in response to oxidative damage.

50 uce a form of programmed cell death known as ferroptosis in starved cancer cells and cancer-bearing m

51 inhibition of cysteine transport to trigger ferroptosis in vitro and slow tumour growth.

52 To suppress ferroptosis in vivo, we generated a novel third-generati

53 duced by Gpx4 ablation exhibited features of ferroptosis, including no caspase-3 activation, no TUNEL

54 adherent epithelial and carcinoma cells from ferroptosis induced by erastin.

55 We further found that ferroptosis inducers inhibit GPX4 by covalently targetin

56 In addition, two representative ferroptosis inducers prevented tumor growth in xenograft

57 and knockdown modulated the lethality of 12 ferroptosis inducers, but not of 11 compounds with other

58 uction of lipid peroxides and is a target of ferroptosis inducers, such as erastin.

59 Erastin, a specific ferroptosis-inducing compound, stimulates heat shock fac

60 ht a common mediator for the lethality of 12 ferroptosis-inducing small molecules.

61 alysis induced by Gpx4 ablation suggest that ferroptosis inhibition by GPX4 is essential for motor ne

62 Consistent with the role of GPX4 as a ferroptosis inhibitor, spinal motor neuron degeneration

63 this study, we report the synthesis of novel ferroptosis inhibitors containing amide and sulfonamide

64 Why certain stimuli trigger ferroptosis instead of another form of cell death, and w

65 mechanism that enables alpha6beta4 to evade ferroptosis involves its ability to protect changes in m

66 esistant to cell death by agents that induce ferroptosis (iron-mediated nonapoptotic cell death).

67 Ferroptosis is a form of nonapoptotic cell death for whi

68 Ferroptosis is a form of programmed cell death that is p

69 Ferroptosis is a form of regulated cell death characteri

70 Ferroptosis is a nonapoptotic, iron-catalyzed form of re

71 Ferroptosis is an iron-dependent form of non-apoptotic c

72 Ferroptosis is an iron-dependent, oxidative form of non-

73 Ferroptosis is an iron-dependent, oxidative, nonapoptoti

74 Ferroptosis is dependent upon intracellular iron, but no

75 Ferroptosis is form of regulated nonapoptotic cell death

76 e 15-lipoxygenase (ALOX15), and SAT1-induced ferroptosis is significantly abrogated in the presence o

77 These data suggest that ferroptosis is the primary cause of FA-AKI and that immu

78 The sensitivity to ferroptosis is tightly linked to numerous biological pro

79 ing of regulated necrosis as they identify a ferroptosis-like cell death in Arabidopsis thaliana.

80 vascular development, was found to involve a ferroptosis-like cell death process.

81 imilarity of ferroptosis in animal cells and ferroptosis-like death in plants suggests that oxidative

82 reversed by the pharmacological inhibitor of ferroptosis, liproxstatin-1.

83 Ferroptosis may also have a tumor-suppressor function th

84 FA-AKI and that immunogenicity secondary to ferroptosis may further worsen the damage, although necr

85 in iron metabolism with important effects on ferroptosis-mediated cancer therapy.

86 o the regulation of polyamine metabolism and ferroptosis-mediated tumor suppression.

87 Finally, ferroptosis mediates postischemic and toxic renal necros

88 glutamate toxicity involves a combination of ferroptosis, necrosis and AIF-dependent apoptosis.

89 drial dysfunction appeared to be involved in ferroptosis of motor neurons induced by Gpx4 ablation.

90 that ferrostatin-1 (Fer-1), an inhibitor of ferroptosis, preserved renal function and decreased hist

91 We sought a common ferroptosis regulator for 15LO.

92 Emerging evidence suggests that ferroptosis represents an ancient vulnerability caused b

93 Thus, activation of ferroptosis results in the nonapoptotic destruction of c

94 Moreover, application of FIP-1 to a model of ferroptosis reveals a change in labile iron pools during

95 to lipoxygenase enzymes, which in turn drive ferroptosis through peroxidation of polyunsaturated fatt

96 rm the potential relevance of metabolism and ferroptosis to tumor suppression by p53.

97 peroxidation and sensitizes cells to undergo ferroptosis upon reactive oxygen species (ROS)-induced s

98 ty to regulate SLC7A11 expression and induce ferroptosis upon reactive oxygen species (ROS)-induced s

99 n of HSF1 and HSPB1 enhances erastin-induced ferroptosis, whereas heat shock pretreatment and overexp

100 vel form of non-apoptotic cell death, called ferroptosis, whereas the mitochondrial isoform of Gpx4 w

101 e the mechanism of lipid peroxidation during ferroptosis, which involves phosphorylase kinase G2 (PHK

102 (ECM) detachment is a physiologic trigger of ferroptosis, which is evaded by alpha6beta4.

103 throughput screening displayed inhibition of ferroptosis with nanomolar activity and was dubbed ferro