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Ferroptosis: Role of lipid peroxidation, iron and ferritinophagy

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Ferroptosis : Role of lipid peroxidation, iron and ferritinophagy. / Latunde-Dada, Gladys O.

In: BIOCHIMICA ET BIOPHYSICA ACTA-GENERAL SUBJECTS, Vol. 1861, No. 8, 01.08.2017, p. 1893-1900.

Research output: Contribution to journalReview article

Harvard

Latunde-Dada, GO 2017, 'Ferroptosis: Role of lipid peroxidation, iron and ferritinophagy', BIOCHIMICA ET BIOPHYSICA ACTA-GENERAL SUBJECTS, vol. 1861, no. 8, pp. 1893-1900. https://doi.org/10.1016/j.bbagen.2017.05.019

APA

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

Vancouver

Latunde-Dada GO. Ferroptosis: Role of lipid peroxidation, iron and ferritinophagy. BIOCHIMICA ET BIOPHYSICA ACTA-GENERAL SUBJECTS. 2017 Aug 1;1861(8):1893-1900. https://doi.org/10.1016/j.bbagen.2017.05.019

Author

Latunde-Dada, Gladys O. / Ferroptosis : Role of lipid peroxidation, iron and ferritinophagy. In: BIOCHIMICA ET BIOPHYSICA ACTA-GENERAL SUBJECTS. 2017 ; Vol. 1861, No. 8. pp. 1893-1900.

Bibtex Download

@article{2a1f19190798463cad75ddf512499983,
title = "Ferroptosis: Role of lipid peroxidation, iron and ferritinophagy",
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.",
keywords = "Apoptosis, Autophagy, Ferritinophagy, Ferroptosis, Necrosis, Peroxidation",
author = "Latunde-Dada, {Gladys O.}",
year = "2017",
month = aug,
day = "1",
doi = "10.1016/j.bbagen.2017.05.019",
language = "English",
volume = "1861",
pages = "1893--1900",
journal = "BIOCHIMICA ET BIOPHYSICA ACTA-GENERAL SUBJECTS",
issn = "0304-4165",
publisher = "Elsevier",
number = "8",

}

RIS (suitable for import to EndNote) Download

TY - JOUR

T1 - Ferroptosis

T2 - Role of lipid peroxidation, iron and ferritinophagy

AU - Latunde-Dada, Gladys O.

PY - 2017/8/1

Y1 - 2017/8/1

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.

AB - 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.

KW - Apoptosis

KW - Autophagy

KW - Ferritinophagy

KW - Ferroptosis

KW - Necrosis

KW - Peroxidation

UR - http://www.scopus.com/inward/record.url?scp=85019715011&partnerID=8YFLogxK

U2 - 10.1016/j.bbagen.2017.05.019

DO - 10.1016/j.bbagen.2017.05.019

M3 - Review article

AN - SCOPUS:85019715011

VL - 1861

SP - 1893

EP - 1900

JO - BIOCHIMICA ET BIOPHYSICA ACTA-GENERAL SUBJECTS

JF - BIOCHIMICA ET BIOPHYSICA ACTA-GENERAL SUBJECTS

SN - 0304-4165

IS - 8

ER -

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