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Ferroptosis: Role of lipid peroxidation, iron and ferritinophagy.
Biochim Biophys Acta Gen Subj. 2017 Aug; 1861(8):1893-1900.BB

Abstract

Ferroptosis is a form of regulated cell death that is dependent on iron and reactive oxygen species (ROS) and is characterized by lipid peroxidation. It is morphologically and biochemically distinct and disparate from other processes of cell death. As ferroptosis is induced by inhibition of cysteine uptake or inactivation of the lipid repair enzyme glutathione peroxidase 4 (GPX4), the process is favored by chemical or mutational inhibition of the cystine/glutamate antiporter and culminates in the accumulation of reactive oxygen species (ROS) in the form of lipid hydroperoxides. Excessive lipid peroxidation leads to death by ferroptosis and the phenotype is accentuated respectively by the repletion and depletion of iron and glutathione in cells. Furthermore, oxidized phosphatidylethanolamines (PE) harbouring arachidonoyl (AA) and adrenoyl moieties (AdA) have been shown as proximate executioners of ferroptosis. Induction of ferroptosis due to cysteine depletion leads to the degradation of ferritin (i.e. ferritinophagy), which releases iron via the NCOA4-mediated autophagy pathway. Evidence of the manifestation of ferroptosis in vivo in iron overload mice mutants is emerging. Thus, a concerted synchronization of iron availability, ROS generation, glutamate excess and cysteine deficit leads to ferroptosis. A number of questions on the molecular mechanisms of some features of ferroptosis are highlighted as subjects for future investigations.

Authors+Show Affiliations

King's College London, Diabetes and Nutritional Sciences Division, Faculty of Life Sciences and Medicine, Franklin-Wilkins Building, London SE1 9NH, United Kingdom. Electronic address: yemisi.latunde-dada@kcl.ac.uk.

Pub Type(s)

Journal Article
Review

Language

eng

PubMed ID

28552631

Citation

Latunde-Dada, Gladys O.. "Ferroptosis: Role of Lipid Peroxidation, Iron and Ferritinophagy." Biochimica Et Biophysica Acta. General Subjects, vol. 1861, no. 8, 2017, pp. 1893-1900.
Latunde-Dada GO. Ferroptosis: Role of lipid peroxidation, iron and ferritinophagy. Biochim Biophys Acta Gen Subj. 2017;1861(8):1893-1900.
Latunde-Dada, G. O. (2017). Ferroptosis: Role of lipid peroxidation, iron and ferritinophagy. Biochimica Et Biophysica Acta. General Subjects, 1861(8), 1893-1900. https://doi.org/10.1016/j.bbagen.2017.05.019
Latunde-Dada GO. Ferroptosis: Role of Lipid Peroxidation, Iron and Ferritinophagy. Biochim Biophys Acta Gen Subj. 2017;1861(8):1893-1900. PubMed PMID: 28552631.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Ferroptosis: Role of lipid peroxidation, iron and ferritinophagy. A1 - Latunde-Dada,Gladys O, Y1 - 2017/05/24/ PY - 2017/01/14/received PY - 2017/05/04/revised PY - 2017/05/23/accepted PY - 2017/5/30/pubmed PY - 2017/10/27/medline PY - 2017/5/30/entrez KW - Apoptosis KW - Autophagy KW - Ferritinophagy KW - Ferroptosis KW - Necrosis KW - Peroxidation SP - 1893 EP - 1900 JF - Biochimica et biophysica acta. General subjects JO - Biochim Biophys Acta Gen Subj VL - 1861 IS - 8 N2 - Ferroptosis is a form of regulated cell death that is dependent on iron and reactive oxygen species (ROS) and is characterized by lipid peroxidation. It is morphologically and biochemically distinct and disparate from other processes of cell death. As ferroptosis is induced by inhibition of cysteine uptake or inactivation of the lipid repair enzyme glutathione peroxidase 4 (GPX4), the process is favored by chemical or mutational inhibition of the cystine/glutamate antiporter and culminates in the accumulation of reactive oxygen species (ROS) in the form of lipid hydroperoxides. Excessive lipid peroxidation leads to death by ferroptosis and the phenotype is accentuated respectively by the repletion and depletion of iron and glutathione in cells. Furthermore, oxidized phosphatidylethanolamines (PE) harbouring arachidonoyl (AA) and adrenoyl moieties (AdA) have been shown as proximate executioners of ferroptosis. Induction of ferroptosis due to cysteine depletion leads to the degradation of ferritin (i.e. ferritinophagy), which releases iron via the NCOA4-mediated autophagy pathway. Evidence of the manifestation of ferroptosis in vivo in iron overload mice mutants is emerging. Thus, a concerted synchronization of iron availability, ROS generation, glutamate excess and cysteine deficit leads to ferroptosis. A number of questions on the molecular mechanisms of some features of ferroptosis are highlighted as subjects for future investigations. SN - 0304-4165 UR - https://www.unboundmedicine.com/medline/citation/28552631/Ferroptosis:_Role_of_lipid_peroxidation_iron_and_ferritinophagy_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0304-4165(17)30171-X DB - PRIME DP - Unbound Medicine ER -