Breakdown of an Ironclad Defense System: The Critical Role of NRF2 in Mediating Ferroptosis DOI Creative Commons
Annadurai Anandhan, Matthew Dodson, Cody J. Schmidlin

et al.

Cell chemical biology, Journal Year: 2020, Volume and Issue: 27(4), P. 436 - 447

Published: April 1, 2020

Ferroptosis is a non-apoptotic mode of regulated cell death that iron and lipid peroxidation dependent. As new mechanistic insight into ferroptotic effectors how they are in different disease contexts uncovered, our understanding the physiological pathological relevance this continues to grow. Along these lines, host pharmacological modulators pathway have been identified, targeting proteins involved homeostasis; generation reduction peroxides; or cystine import glutathione metabolism. Also, note, many components ferroptosis cascade target genes transcription factor nuclear erythroid 2-related 2 (NRF2), indicating its critical role mediating response. In review, we discuss vitro, vivo, clinical evidence disease, including brief discussion upstream mediators cascade, NRF2, treat ferroptosis-driven diseases.

Language: Английский

Ferroptosis: A Regulated Cell Death Nexus Linking Metabolism, Redox Biology, and Disease DOI Creative Commons
Brent R. Stockwell, José Pedro Friedmann Angeli, Hülya Bayır

et al.

Cell, Journal Year: 2017, Volume and Issue: 171(2), P. 273 - 285

Published: Oct. 1, 2017

Language: Английский

Citations

5504

Molecular mechanisms of cell death: recommendations of the Nomenclature Committee on Cell Death 2018 DOI Creative Commons
Lorenzo Galluzzi, Ilio Vitale, Stuart A. Aaronson

et al.

Cell Death and Differentiation, Journal Year: 2018, Volume and Issue: 25(3), P. 486 - 541

Published: Jan. 23, 2018

Over the past decade, Nomenclature Committee on Cell Death (NCCD) has formulated guidelines for definition and interpretation of cell death from morphological, biochemical, functional perspectives. Since field continues to expand novel mechanisms that orchestrate multiple pathways are unveiled, we propose an updated classification subroutines focusing mechanistic essential (as opposed correlative dispensable) aspects process. As provide molecularly oriented definitions terms including intrinsic apoptosis, extrinsic mitochondrial permeability transition (MPT)-driven necrosis, necroptosis, ferroptosis, pyroptosis, parthanatos, entotic death, NETotic lysosome-dependent autophagy-dependent immunogenic cellular senescence, mitotic catastrophe, discuss utility neologisms refer highly specialized instances these processes. The mission NCCD is a widely accepted nomenclature in support continued development field.

Language: Английский

Citations

5351

FSP1 is a glutathione-independent ferroptosis suppressor DOI
Sebastian Doll, Florêncio Porto Freitas, Ron Shah

et al.

Nature, Journal Year: 2019, Volume and Issue: 575(7784), P. 693 - 698

Published: Oct. 21, 2019

Language: Английский

Citations

2366

Ferroptosis as a target for protection against cardiomyopathy DOI Creative Commons
Xuexian Fang, Hao Wang, Dan Han

et al.

Proceedings of the National Academy of Sciences, Journal Year: 2019, Volume and Issue: 116(7), P. 2672 - 2680

Published: Jan. 28, 2019

Significance Nonapoptotic cell death-induced tissue damage has been implicated in a variety of diseases, including neurodegenerative disorder, inflammation, and stroke. In this study, we demonstrate that ferroptosis, newly defined iron-dependent death, mediates both chemotherapy- ischemia/reperfusion-induced cardiomyopathy. RNA-sequencing analysis revealed up-regulation heme oxygenase 1 by doxorubicin as major mechanism ferroptotic As result, degrades releases free iron cardiomyocytes, which turn leads to generation oxidized lipids the mitochondria membrane. Most importantly, chelation therapy pharmacologically blocking ferroptosis could significantly alleviate cardiomyopathy mice. These findings suggest targeting strategy for treating deadly heart disease.

Language: Английский

Citations

1638

Role of Mitochondria in Ferroptosis DOI Creative Commons
Minghui Gao, Jun-Mei Yi, Jiajun Zhu

et al.

Molecular Cell, Journal Year: 2018, Volume and Issue: 73(2), P. 354 - 363.e3

Published: Dec. 20, 2018

Language: Английский

Citations

1562

Recent Progress in Ferroptosis Inducers for Cancer Therapy DOI
Chen Liang, Xinglin Zhang, Mengsu Yang

et al.

Advanced Materials, Journal Year: 2019, Volume and Issue: 31(51)

Published: Oct. 8, 2019

Abstract Ferroptosis is a newly discovered form of regulated cell death that the nexus between metabolism, redox biology, and human health. Emerging evidence shows potential triggering ferroptosis for cancer therapy, particularly eradicating aggressive malignancies are resistant to traditional therapies. Recently, there has been great deal effort design develop anticancer drugs based on induction. Recent advances ferroptosis‐inducing agents at intersection chemistry, materials science, biology presented. The basis summarized first highlight feasibility characteristics therapy. A literature review inducers (including small molecules nanomaterials) then presented delineate their design, action mechanisms, applications. Finally, some considerations research spotlighted, followed by discussion challenges future development directions this burgeoning field.

Language: Английский

Citations

1271

Selenium Utilization by GPX4 Is Required to Prevent Hydroperoxide-Induced Ferroptosis DOI Creative Commons

Irina Ingold,

Carsten Berndt,

Sabine Schmitt

et al.

Cell, Journal Year: 2017, Volume and Issue: 172(3), P. 409 - 422.e21

Published: Dec. 28, 2017

Language: Английский

Citations

1266

Role of GPX4 in ferroptosis and its pharmacological implication DOI

Tobias Seibt,

Bettina Proneth, Marcus Conrad

et al.

Free Radical Biology and Medicine, Journal Year: 2018, Volume and Issue: 133, P. 144 - 152

Published: Sept. 13, 2018

Language: Английский

Citations

1122

The development of the concept of ferroptosis DOI
Tal Hirschhorn, Brent R. Stockwell

Free Radical Biology and Medicine, Journal Year: 2018, Volume and Issue: 133, P. 130 - 143

Published: Sept. 27, 2018

Language: Английский

Citations

871

Ischemia-induced ACSL4 activation contributes to ferroptosis-mediated tissue injury in intestinal ischemia/reperfusion DOI Creative Commons
Li Yang,

Dongcheng Feng,

Zhanyu Wang

et al.

Cell Death and Differentiation, Journal Year: 2019, Volume and Issue: 26(11), P. 2284 - 2299

Published: Feb. 8, 2019

Ferroptosis is a recently identified form of regulated cell death defined by the iron-dependent accumulation lipid reactive oxygen species. has been studied in various diseases such as cancer, Parkinson's disease, and stroke. However, exact function mechanism ferroptosis ischemia/reperfusion (I/R) injury, especially intestine, remains unknown. Considering unique conditions required for ferroptosis, we hypothesize that ischemia promotes immediately after intestinal reperfusion. In contrast to conventional strategies employed I/R studies, focused on ischemic phase. Here verified assessing proferroptotic changes along with protein peroxidation levels during The inhibition liproxstatin-1 ameliorated I/R-induced injury. Acyl-CoA synthetase long-chain family member 4 (ACSL4), which key enzyme regulates composition, shown contribute execution but its role needs clarification. present study, used rosiglitazone (ROSI) siRNA inhibit ischemia/hypoxia-induced ACSL4 vivo vitro. results demonstrated before reperfusion protected against death. Further investigation revealed special 1 (Sp1) was crucial transcription factor increased binding promoter region. Collectively, this study demonstrates closely associated critical lethal process. Sp1 an important promoting expression. These suggest effective mechanistic approach injury prevention treatment.

Language: Английский

Citations

717