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Revisiting Tumors and the Cardiovascular System: Mechanistic Intersections and Divergences in Ferroptosis
Ferroptosis was recently identified as an iron-dependent regulatory necrosis process mediated by polyunsaturated fatty acid (PUFA) peroxidation. The pivotal events related to oxidative stress in ferroptosis include direct or indirect glutathione peroxidase 4 (GPX4) inhibition, ferrous iron overload,...
Autores principales: | , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Hindawi
2020
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7450308/ https://www.ncbi.nlm.nih.gov/pubmed/32908642 http://dx.doi.org/10.1155/2020/9738143 |
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author | Wang, Yani Peng, Xiang Zhang, Maomao Jia, Ying Yu, Bo Tian, Jinwei |
author_facet | Wang, Yani Peng, Xiang Zhang, Maomao Jia, Ying Yu, Bo Tian, Jinwei |
author_sort | Wang, Yani |
collection | PubMed |
description | Ferroptosis was recently identified as an iron-dependent regulatory necrosis process mediated by polyunsaturated fatty acid (PUFA) peroxidation. The pivotal events related to oxidative stress in ferroptosis include direct or indirect glutathione peroxidase 4 (GPX4) inhibition, ferrous iron overload, and lipid peroxidation. The links between ferroptosis and multiple pathological processes including tumor and cardiovascular system disease have become increasingly apparent, and the mechanisms and compounds involved in ferroptosis, such as reduction of coenzyme Q(10) (ubiquinone/CoQ(10)), are gradually emerging. Current reports have revealed crossroads between ferroptosis and other multiple responses. This overview of the current research illuminates the mechanisms involving ferroptosis-related compounds and emphasizes the crosstalk between ferroptosis and other responses, including mitochondrial damage, endoplasmic reticulum stress (ER stress), autophagy, and the release of damage-associated molecular patterns (DAMPs), to reveal the intersections of regulatory mechanisms. This review also outlines the discovery, characterization, and pathological relevance of ferroptosis and notes controversial elements in ferroptosis-related mechanisms, such as nuclear factor E2-related factor 2 (Nrf2), sequestosome 1 (p62/SQSTM1), and heat shock protein family A member 5 (HSPA5). We hope our inferences will supply a partial reference for disorder prevention and treatment. |
format | Online Article Text |
id | pubmed-7450308 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2020 |
publisher | Hindawi |
record_format | MEDLINE/PubMed |
spelling | pubmed-74503082020-09-08 Revisiting Tumors and the Cardiovascular System: Mechanistic Intersections and Divergences in Ferroptosis Wang, Yani Peng, Xiang Zhang, Maomao Jia, Ying Yu, Bo Tian, Jinwei Oxid Med Cell Longev Review Article Ferroptosis was recently identified as an iron-dependent regulatory necrosis process mediated by polyunsaturated fatty acid (PUFA) peroxidation. The pivotal events related to oxidative stress in ferroptosis include direct or indirect glutathione peroxidase 4 (GPX4) inhibition, ferrous iron overload, and lipid peroxidation. The links between ferroptosis and multiple pathological processes including tumor and cardiovascular system disease have become increasingly apparent, and the mechanisms and compounds involved in ferroptosis, such as reduction of coenzyme Q(10) (ubiquinone/CoQ(10)), are gradually emerging. Current reports have revealed crossroads between ferroptosis and other multiple responses. This overview of the current research illuminates the mechanisms involving ferroptosis-related compounds and emphasizes the crosstalk between ferroptosis and other responses, including mitochondrial damage, endoplasmic reticulum stress (ER stress), autophagy, and the release of damage-associated molecular patterns (DAMPs), to reveal the intersections of regulatory mechanisms. This review also outlines the discovery, characterization, and pathological relevance of ferroptosis and notes controversial elements in ferroptosis-related mechanisms, such as nuclear factor E2-related factor 2 (Nrf2), sequestosome 1 (p62/SQSTM1), and heat shock protein family A member 5 (HSPA5). We hope our inferences will supply a partial reference for disorder prevention and treatment. Hindawi 2020-08-17 /pmc/articles/PMC7450308/ /pubmed/32908642 http://dx.doi.org/10.1155/2020/9738143 Text en Copyright © 2020 Yani Wang et al. http://creativecommons.org/licenses/by/4.0/ This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. |
spellingShingle | Review Article Wang, Yani Peng, Xiang Zhang, Maomao Jia, Ying Yu, Bo Tian, Jinwei Revisiting Tumors and the Cardiovascular System: Mechanistic Intersections and Divergences in Ferroptosis |
title | Revisiting Tumors and the Cardiovascular System: Mechanistic Intersections and Divergences in Ferroptosis |
title_full | Revisiting Tumors and the Cardiovascular System: Mechanistic Intersections and Divergences in Ferroptosis |
title_fullStr | Revisiting Tumors and the Cardiovascular System: Mechanistic Intersections and Divergences in Ferroptosis |
title_full_unstemmed | Revisiting Tumors and the Cardiovascular System: Mechanistic Intersections and Divergences in Ferroptosis |
title_short | Revisiting Tumors and the Cardiovascular System: Mechanistic Intersections and Divergences in Ferroptosis |
title_sort | revisiting tumors and the cardiovascular system: mechanistic intersections and divergences in ferroptosis |
topic | Review Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7450308/ https://www.ncbi.nlm.nih.gov/pubmed/32908642 http://dx.doi.org/10.1155/2020/9738143 |
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