324:
269:
158:, thus causing decreased intracellular glutathione (GSH) levels. Given that GSH is necessary for GPX4 function, depletion of this cofactor can lead to ferroptotic cell death. Oxytosis/ferroptosis can also be induced through inhibition of GPX4, as is the molecular mechanism of action of RSL3, ML162, and ML210. In some cells, FSP1 compensates for loss of GPX4 activity, and both GPX4 and FSP1 must be inhibited simultaneously to induce oxytosis/ferroptosis.
389:. These cells also exhibited an autophagic cycle independent of ferroptotic activity, indicating that the two different forms of cell death could be controlled to activate at specific times following treatment. Furthermore, intratumor bacteria may scavenge iron by producing iron siderophores, which indirectly protect tumor cells from ferroptosis, emphasizing the need for ferroptosis inducers (thiostrepton) for cancer treatment.
293:. Two new studies show that oxytosis/ferroptosis contributes to neuronal death after intracerebral hemorrhage. Neurons that are degraded through oxytosis/ferroptosis release lipid metabolites from inside the cell body. The lipid metabolites are harmful to surrounding neurons, causing inflammation in the brain. Inflammation is a pathological feature of
312:, can influence how readily a neuron undergoes cell death. The presence of ATF4 promotes resistance in cells against oxytosis/ferroptosis. However, this resistance can cause other diseases, such as cancer, to progress and become malignant. While ATF4 provides resistance oxytosis/ferroptosis, an abundance of ATF4 causes neurodegeneration.
304:
promote Gpx4 activity, consequently inhibiting oxytosis/ferroptosis and preventing inflammation in brain regions. In the experimental group of mice that were manipulated to have decreased Gpx4 levels, mice were observed to have cognitive impairment and neurodegeneration of hippocampal neurons, again
280:
connections that are used more often are kept intact and promoted, while synaptic connections that are rarely used are subject to degradation. Elevated levels of synaptic connection loss and degradation of neurons are linked to neurodegenerative diseases. More recently, oxytosis/ferroptosis has been
259:
through the formation of the apoptosome. Once caspase-9 is activated, it can cleave and activate caspase-3 resulting in cell death. Notably, apoptosis does not release intracellular fluid as neurons that are degraded though oxytosis/ferroptosis do. During oxytosis/ferroptosis, neurons release lipid
46:
Researchers have identified roles in which oxytosis/ferroptosis can contribute to the medical field, such as the development of cancer therapies. Ferroptosis activation plays a regulatory role on growth of tumor cells in the human body. However, the positive effects of oxytosis/ferroptosis could be
42:
and Scott J. Dixon coined the term ferroptosis and described several of its key features. Pamela Maher and David
Schubert discovered the process in 2001 and called it oxytosis. While they did not describe the involvement of iron at the time, oxytosis and ferroptosis are today thought to be the same
38:-dependent antioxidant defenses, resulting in unchecked lipid peroxidation and eventual cell death. Lipophilic antioxidants and iron chelators can prevent ferroptotic cell death. Although the connection between iron and lipid peroxidation has been appreciated for years, it was not until 2012 that
230:
During embryonic development, the absence of NGF activates apoptosis by decreasing the activity of the signaling pathways normally activated by NGF. Without NGF, the neurons of the sympathetic nervous system begin to atrophy, glucose uptake rates fall, and the rates of protein synthesis and gene
51:
in the human body. Since oxytosis/ferroptosis is a form of regulated cell death, some of the molecules that regulate oxytosis/ferroptosis are involved in metabolic pathways that regulate cysteine exploitation, glutathione state, nicotinamide adenine dinucleotide phosphate (NADP) function, lipid
952:
Mai, Trang Thi; Hamaï, Ahmed; Hienzsch, Antje; Cañeque, Tatiana; Müller, Sebastian; Wicinski, Julien; Cabaud, Olivier; Leroy, Christine; David, Amandine; Acevedo, Verónica; Ryo, Akihide; Ginestier, Christophe; Birnbaum, Daniel; Charafe-Jauffret, Emmanuelle; Codogno, Patrice; Mehrpour, Maryam;
175:
has been used to observe the morphological changes that cells undergo during oxytosis/ferroptosis. Initially the cell contracts and then begins to swell. Perinuclear lipid assembly is observed immediately before oxytosis/ferroptosis occurs. After the process is complete, lipid droplets are
380:
These forms of cancer have been hypothesized to be highly sensitive to oxytosis/ferroptosis induction. An upregulation of iron levels has also been seen to induce oxytosis/ferroptosis in certain types of cancer, such as breast cancer. Breast cancer cells have exhibited vulnerability to
169:(dPUFA), which have deuterium in place of the bis-allylic hydrogens, can prevent cell death induced by erastin or RSL3. These deuterated PUFAs effectively inhibit ferroptosis and various chronic degenerative diseases associated with ferroptosis.
80:), a glutathione-dependent hydroperoxidase that converts lipid peroxides into non-toxic lipid alcohols. Recently, a second parallel protective pathway was independently discovered by two labs that involves the oxidoreductase FSP1 (also known as
192:. This process occurs continuously within mammalian nervous system processes that begin at fetal development and continue through adult life. Apoptotic death is crucial for the correct population size of neuronal and
68:
via iron is crucial for the generation of reactive oxygen species and this feature can be exploited by sequestering iron in lysosomes. Oxidation of phospholipids can occur when free radicals abstract
72:
from a lipid molecule (typically affecting polyunsaturated fatty acids), thereby promoting their oxidation. The primary cellular mechanism of protection against oxytosis/ferroptosis is mediated by
335:
Preliminary reports suggest that oxytosis/ferroptosis may be a means through which tumor cells can be killed. Oxytosis/ferroptosis has been implicated in several types of cancer, including:
1687:"Ultrastructural Characteristics of Neuronal Death and White Matter Injury in Mouse Brain Tissues After Intracerebral Hemorrhage: Coexistence of Ferroptosis, Autophagy, and Necrosis"
392:
Notably, not all cancers are necessarily sensitive to oxytosis/ferroptosis induction. For instance, one study has demonstrated that oxytosis/ferroptosis in polymorphonuclear
138:)-RSL3, ML162, and ML210 are known inhibitors of tumor cell growth via induction of oxytosis/ferroptosis. These compounds do not trigger apoptosis and therefore do not cause
111:
323:
1738:"Traumatic Brain Injury: Ultrastructural Features in Neuronal Ferroptosis, Glial Cell Activation and Polarization, and Blood-Brain Barrier Breakdown"
220:
1499:"Ablation of ferroptosis regulator glutathione peroxidase 4 in forebrain neurons promotes cognitive impairment and neurodegeneration"
604:"On the Mechanism of Cytoprotection by Ferrostatin-1 and Liproxstatin-1 and the Role of Lipid Peroxidation in Ferroptotic Cell Death"
1906:
1290:"Lipid Metabolism Regulates Oxidative Stress and Ferroptosis in RAS-Driven Cancers: A Perspective on Cancer Progression and Therapy"
453:
Shirlee Tan, Bentham
Science Publisher; David Schubert, Bentham Science Publisher; Pamela Maher, Bentham Science Publisher (2001).
91:, thereby generating a potent lipophilic antioxidant that suppresses the propagation of lipid peroxides. A similar mechanism for a
1789:"Ferroptosis and autophagy induced cell death occur independently after siramesine and lapatinib treatment in breast cancer cells"
196:
cells. Similarly to oxytosis/ferroptosis, deficiencies in apoptotic processes can result in many health complications, including
393:
1901:
60:
The hallmark feature of oxytosis/ferroptosis is the iron-dependent accumulation of oxidatively damaged phospholipids (i.e.,
1074:
286:
212:
155:
1848:"Bacterial Iron Siderophore Drives Tumor Survival and Ferroptosis Resistance in a Biofilm‐Tumor Spheroid Coculture Model"
315:
Recent studies have suggested that oxytosis/ferroptosis contributes to neuronal cell death after traumatic brain injury.
247:(Bcl-2) proteins prevents NGF withdrawal-induced death. However, overexpression of a separate, pro-apoptotic Bcl-2 gene,
150:
is also necessary for small-molecule oxytosis/ferroptosis induction; therefore, these compounds can be inhibited by iron
143:
268:
1911:
300:
In a study performed using mice, it was found that the absence of Gpx4 promoted oxytosis/ferroptosis. Foods high in
1595:
Ryan, Sean K.; Ugalde, Cathryn L.; Rolland, Anne-Sophie; Skidmore, John; Devos, David; Hammond, Timothy R. (2023).
707:"Lipid peroxidation initiated by superoxide-dependent hydroxyl radicals using complexed iron and hydrogen peroxide"
248:
224:
204:
162:
223:(Raf-MEK-ERK) signaling pathways. This occurs during normal development which promotes neuronal growth in the
110:
260:
metabolites from inside the cell body. This is a key difference between oxytosis/ferroptosis and apoptosis.
92:
756:"Using the Oxytosis/Ferroptosis Pathway to Understand and Treat Age-Associated Neurodegenerative Diseases"
397:
344:
294:
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282:
216:
23:
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Kraft VA, Bezjian CT, Pfeiffer S, Ringelstetter L, Müller C, Zandkarimi F, et al. (January 2020).
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30:, and is genetically and biochemically distinct from other forms of regulated cell death such as
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from the mitochondria. In a surviving sympathetic neuron, the overexpression of anti-apoptotic
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Within the study of neuronal apoptosis, most research has been conducted on the neurons of the
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Yeung, Yoyo Wing Suet; Ma, Yeping; Deng, Yanlin; Khoo, Bee Luan; Chua, Song Lin (2024-08-12).
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Doll S, Freitas FP, Shah R, Aldrovandi M, da Silva MC, Ingold I, et al. (November 2019).
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Dixon SJ, Lemberg KM, Lamprecht MR, Skouta R, Zaitsev EM, Gleason CE, et al. (May 2012).
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Ma S, Dielschneider RF, Henson ES, Xiao W, Choquette TR, Blankstein AR, et al. (2017).
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Bersuker K, Hendricks JM, Li Z, Magtanong L, Ford B, Tang PH, et al. (November 2019).
207:. In order for these neurons to survive and innervate their target tissues, they must have
1143:"GTP Cyclohydrolase 1/Tetrahydrobiopterin Counteract Ferroptosis through Lipid Remodeling"
359:
146:(PARP) cleavage. Instead, oxytosis/ferroptosis causes changes in mitochondrial phenotype.
61:
39:
1239:
Eaton JK, Furst L, Ruberto RA, Moosmayer D, Hilpmann A, Ryan MJ, et al. (May 2020).
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Zilka O, Shah R, Li B, Friedmann Angeli JP, Griesser M, Conrad M, Pratt DA (March 2017).
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1192:"Metabolic determinants of cancer cell sensitivity to canonical ferroptosis inducers"
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Soula M, Weber RA, Zilka O, Alwaseem H, La K, Yen F, et al. (December 2020).
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potentially neutralized by its disruption of metabolic pathways and disruption of
1813:
1450:"Programmed cell death during neuronal development: the sympathetic neuron model"
1514:
369:
48:
35:
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1241:"Selective covalent targeting of GPX4 using masked nitrile-oxide electrophiles"
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188:, which results in cell breakage into small, apoptotic bodies taken up through
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moonlighting as a diffusable antioxidant was discovered in the same year for
84:). Their findings indicate that FSP1 enzymatically reduces non-mitochondrial
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activation occurs through an in-vitro pathway beginning with the release of
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Li Q, Weiland A, Chen X, Lan X, Han X, Durham F, et al. (July 2018).
1015:"The CoQ oxidoreductase FSP1 acts parallel to GPX4 to inhibit ferroptosis"
732:
877:
69:
1465:
978:
955:"Salinomycin kills cancer stem cells by sequestering iron in lysosomes"
424:
419:
277:
232:
119:
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Li Q, Han X, Lan X, Gao Y, Wan J, Durham F, et al. (April 2017).
1288:
Bartolacci, C.; Andreani, C.; El-Gammal, Y.; Scaglioni, P. P. (2021).
808:"The Role of Ferroptosis in Cancer Development and Treatment Response"
276:
Neural connections are constantly changing within the nervous system.
1597:"Therapeutic inhibition of ferroptosis in neurodegenerative disease"
231:
expression slow. Apoptotic death from NGF withdrawal also requires
322:
267:
109:
81:
1546:
Weiland A, Wang Y, Wu W, Lan X, Han X, Li Q, Wang J (July 2019).
860:
Hao S, Liang B, Huang Q, Dong S, Wu Z, He W, Shi M (April 2018).
806:
Lu B, Chen XB, Ying MD, He QJ, Cao J, Yang B (12 January 2018).
658:"Ferroptosis: an iron-dependent form of nonapoptotic cell death"
414:
328:
309:
184:
Another form of cell death that occurs in the nervous system is
147:
77:
73:
1638:"Inhibition of neuronal ferroptosis protects hemorrhagic brain"
1497:
Hambright WS, Fonseca RS, Chen L, Na R, Ran Q (August 2017).
305:
linking oxytosis/ferroptosis to neurodegenerative diseases.
1736:
Qin D, Wang J, Le A, Wang TJ, Chen X, Wang J (April 2021).
1339:
Jiang, Xuejun; Stockwell, Brent R.; Conrad, Marcus (2021).
308:
Similarly, presence of transcription factors, specifically
176:
redistributed throughout the cell (see GIF on right side).
26:
dependent on iron and characterized by the accumulation of
1075:"FSP1 is a glutathione-independent ferroptosis suppressor"
211:(NGF). Normally, NGF binds to a tyrosine kinase receptor,
34:. Oxytosis/ferroptosis is initiated by the failure of the
448:
446:
327:
Initiation of ferroptosis by inhibition of Xc- system of
1443:
1441:
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1435:
1433:
1341:"Ferroptosis: mechanisms, biology and role in disease"
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215:, which activates phosphatidylinositol 3-kinase-Akt (
1548:"Ferroptosis and Its Role in Diverse Brain Diseases"
114:Human prostate cancer cells undergoing ferroptosis
855:
853:
548:
546:
455:"Oxytosis: A Novel Form of Programmed Cell Death"
281:linked to diverse brain diseases, in particular,
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272:Induction of neurodegeneration by Ferroptosis
180:Comparison to apoptosis in the nervous system
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400:releases oxidized lipids that contribute to
953:xRodriguez, Raphaël Rodriguez (Oct 2017).
503:"Ferroptosis: Death by Lipid Peroxidation"
381:oxytosis/ferroptosis via a combination of
255:. Cytochrome c promotes the activation of
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154:. Erastin acts through inhibition of the
103:), a product of the rate-limiting enzyme
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1345:Nature Reviews. Molecular Cell Biology
459:Current Topics in Medicinal Chemistry
221:extracellular signal-regulated kinase
7:
559:Cellular and Molecular Life Sciences
501:Yang WS, Stockwell BR (March 2016).
52:peroxidation, and iron homeostasis.
862:"Metabolic networks in ferroptosis"
1601:Trends in Pharmacological Sciences
1448:Kristiansen M, Ham J (July 2014).
1294:Frontiers in Molecular Biosciences
754:Maher, Pamela (17 December 2020).
319:Potential role in cancer treatment
14:
1394:The American Journal of Pathology
394:myeloid-derived suppressor cells
350:Pancreatic ductal adenocarcinoma
235:activity. Upon NGF withdrawal,
1454:Cell Death and Differentiation
772:10.1016/j.chembiol.2020.10.010
553:Cao JY, Dixon SJ (June 2016).
297:and intracerebral hemorrhage.
1:
1406:10.1016/S0002-9440(10)64779-7
287:amyotrophic lateral sclerosis
156:cystine/glutamate transporter
16:Type of programmed cell death
1814:10.1371/journal.pone.0182921
724:10.1016/0014-5793(84)81134-5
251:, stimulates the release of
144:poly (ADP-ribose) polymerase
1515:10.1016/j.redox.2017.01.021
911:Cell Biology and Toxicology
705:Gutteridge JM (July 1984).
555:"Mechanisms of ferroptosis"
163:polyunsaturated fatty acids
1928:
1614:10.1016/j.tips.2023.07.007
1357:10.1038/s41580-020-00324-8
1159:10.1021/acscentsci.9b01063
923:10.1007/s10565-019-09496-2
674:10.1016/j.cell.2012.03.042
620:10.1021/acscentsci.7b00028
225:sympathetic nervous system
205:superior cervical ganglion
1654:10.1172/jci.insight.90777
1564:10.1007/s12035-018-1403-3
1390:"Mechanisms of apoptosis"
1388:Reed JC (November 2000).
1307:10.3389/fmolb.2021.706650
1257:10.1038/s41589-020-0501-5
1208:10.1038/s41589-020-0613-y
1102:10.1038/s41586-019-1707-0
1039:10.1038/s41586-019-1705-2
812:Frontiers in Pharmacology
571:10.1007/s00018-016-2194-1
519:10.1016/j.tcb.2015.10.014
1907:Medical aspects of death
1704:10.3389/fneur.2018.00581
825:10.3389/fphar.2017.00992
471:10.2174/1568026013394741
118:Small molecules such as
74:glutathione peroxidase 4
1245:Nature Chemical Biology
1196:Nature Chemical Biology
1861:10.1002/advs.202404467
1691:Frontiers in Neurology
1552:Molecular Neurobiology
507:Trends in Cell Biology
398:tumor microenvironment
345:Acute myeloid leukemia
332:
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64:). The implication of
43:cell death mechanism.
1902:Programmed cell death
1755:10.3390/cells10051009
365:Renal cell carcinomas
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245:B-cell CLL/lymphoma 2
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24:programmed cell death
878:10.3892/ol.2018.8066
20:Oxytosis/ferroptosis
1805:2017PLoSO..1282921M
1466:10.1038/cdd.2014.47
1147:ACS Central Science
1094:2019Natur.575..693D
1031:2019Natur.575..688B
971:2017NatCh...9.1025M
608:ACS Central Science
565:(11–12): 2195–209.
295:Alzheimer’s disease
291:Parkinson's disease
283:Alzheimer's disease
209:nerve growth factor
97:tetrahydrobiopterin
1912:Cellular processes
1887:KEGG pathway entry
979:10.1038/nchem.2778
402:immune suppression
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161:Replacing natural
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482:. Retrieved
462:
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375:Glioblastoma
334:
314:
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241:cytochrome c
229:
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190:phagocytosis
183:
171:
165:(PUFA) with
160:
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1642:JCI Insight
49:homeostasis
36:glutathione
1896:Categories
484:2023-03-15
437:References
383:siramesine
264:In neurons
86:coenzyme Q
1870:2198-3844
1128:204833583
939:254369328
430:XJB-5-131
387:lapatinib
302:vitamin E
257:caspase-9
237:caspase-3
186:apoptosis
152:chelators
140:chromatin
128:sorafenib
70:electrons
56:Mechanism
32:apoptosis
1833:28827805
1793:PLOS ONE
1774:33923370
1723:30065697
1672:28405617
1623:37657967
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638:28386601
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537:26653790
479:11895126
408:See also
331:activity
278:Synaptic
217:PI3K-Akt
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1801:Bibcode
1765:8146242
1714:6056664
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1663:5374066
1573:6506411
1524:5312549
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1415:1885741
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1217:8299533
1168:6978838
1090:Bibcode
1048:6883167
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988:5890907
967:Bibcode
887:5844144
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733:6086389
683:3367386
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425:Erastin
420:SLC7A11
396:in the
355:Ovarian
233:caspase
120:erastin
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340:Breast
289:, and
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1742:Cells
1124:S2CID
1078:(PDF)
935:S2CID
737:S2CID
194:glial
82:AIFM2
1866:ISSN
1829:PMID
1770:PMID
1719:PMID
1668:PMID
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1420:PMID
1371:PMID
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1116:PMID
1053:PMID
993:PMID
927:PMID
892:PMID
840:PMID
786:PMID
729:PMID
688:PMID
662:Cell
634:PMID
585:PMID
533:PMID
475:PMID
415:GPX4
385:and
370:Lung
329:GPX4
310:ATF4
213:TrkA
148:Iron
130:, (1
105:GCH1
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1760:PMC
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1106:hdl
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