The emerging role of ferroptosis in intestinal disease
Abstract Ferroptosis is a newly recognised type of regulated cell death (RCD) characterised by iron-dependent accumulation of lipid peroxidation. It is significantly distinct from other RCDs at the morphological, biochemical, and genetic levels. Recent reports have implicated ferroptosis in multiple...
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2021-03-01
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Series: | Cell Death and Disease |
Online Access: | https://doi.org/10.1038/s41419-021-03559-1 |
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doaj-456316b6438a4236b93765a9fd725b312021-03-21T12:05:31ZengNature Publishing GroupCell Death and Disease2041-48892021-03-0112411210.1038/s41419-021-03559-1The emerging role of ferroptosis in intestinal diseaseShu Xu0Yao He1Lihui Lin2Peng Chen3Minhu Chen4Shenghong Zhang5Division of Gastroenterology, The First Affiliated Hospital, Sun Yat-sen UniversityDivision of Gastroenterology, The First Affiliated Hospital, Sun Yat-sen UniversityDivision of Gastroenterology, The First Affiliated Hospital, Sun Yat-sen UniversityDivision of Gastroenterology, The First Affiliated Hospital, Sun Yat-sen UniversityDivision of Gastroenterology, The First Affiliated Hospital, Sun Yat-sen UniversityDivision of Gastroenterology, The First Affiliated Hospital, Sun Yat-sen UniversityAbstract Ferroptosis is a newly recognised type of regulated cell death (RCD) characterised by iron-dependent accumulation of lipid peroxidation. It is significantly distinct from other RCDs at the morphological, biochemical, and genetic levels. Recent reports have implicated ferroptosis in multiple diseases, including neurological disorders, kidney injury, liver diseases, and cancer. Ferroptotic cell death has also been associated with dysfunction of the intestinal epithelium, which contributes to several intestinal diseases. Research on ferroptosis may provide a new understanding of intestinal disease pathogenesis that benefits clinical treatment. In this review, we provide an overview of ferroptosis and its underlying mechanisms, then describe its emerging role in intestinal diseases, including intestinal ischaemia/reperfusion (I/R) injury, inflammatory bowel disease (IBD), and colorectal cancer (CRC).https://doi.org/10.1038/s41419-021-03559-1 |
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DOAJ |
language |
English |
format |
Article |
sources |
DOAJ |
author |
Shu Xu Yao He Lihui Lin Peng Chen Minhu Chen Shenghong Zhang |
spellingShingle |
Shu Xu Yao He Lihui Lin Peng Chen Minhu Chen Shenghong Zhang The emerging role of ferroptosis in intestinal disease Cell Death and Disease |
author_facet |
Shu Xu Yao He Lihui Lin Peng Chen Minhu Chen Shenghong Zhang |
author_sort |
Shu Xu |
title |
The emerging role of ferroptosis in intestinal disease |
title_short |
The emerging role of ferroptosis in intestinal disease |
title_full |
The emerging role of ferroptosis in intestinal disease |
title_fullStr |
The emerging role of ferroptosis in intestinal disease |
title_full_unstemmed |
The emerging role of ferroptosis in intestinal disease |
title_sort |
emerging role of ferroptosis in intestinal disease |
publisher |
Nature Publishing Group |
series |
Cell Death and Disease |
issn |
2041-4889 |
publishDate |
2021-03-01 |
description |
Abstract Ferroptosis is a newly recognised type of regulated cell death (RCD) characterised by iron-dependent accumulation of lipid peroxidation. It is significantly distinct from other RCDs at the morphological, biochemical, and genetic levels. Recent reports have implicated ferroptosis in multiple diseases, including neurological disorders, kidney injury, liver diseases, and cancer. Ferroptotic cell death has also been associated with dysfunction of the intestinal epithelium, which contributes to several intestinal diseases. Research on ferroptosis may provide a new understanding of intestinal disease pathogenesis that benefits clinical treatment. In this review, we provide an overview of ferroptosis and its underlying mechanisms, then describe its emerging role in intestinal diseases, including intestinal ischaemia/reperfusion (I/R) injury, inflammatory bowel disease (IBD), and colorectal cancer (CRC). |
url |
https://doi.org/10.1038/s41419-021-03559-1 |
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