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Ferroptosis in infection, inflammation, and immunity

Ferroptosis is a type of regulated necrosis that is triggered by a combination of iron toxicity, lipid peroxidation, and plasma membrane damage. The upstream inducers of ferroptosis can be divided into two categories (biological versus chemical) and activate two major pathways (the extrinsic/transpo...

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Detalles Bibliográficos
Autores principales: Chen, Xin, Kang, Rui, Kroemer, Guido, Tang, Daolin
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Rockefeller University Press 2021
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8126980/
https://www.ncbi.nlm.nih.gov/pubmed/33978684
http://dx.doi.org/10.1084/jem.20210518
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author Chen, Xin
Kang, Rui
Kroemer, Guido
Tang, Daolin
author_facet Chen, Xin
Kang, Rui
Kroemer, Guido
Tang, Daolin
author_sort Chen, Xin
collection PubMed
description Ferroptosis is a type of regulated necrosis that is triggered by a combination of iron toxicity, lipid peroxidation, and plasma membrane damage. The upstream inducers of ferroptosis can be divided into two categories (biological versus chemical) and activate two major pathways (the extrinsic/transporter versus the intrinsic/enzymatic pathways). Excessive or deficient ferroptotic cell death is implicated in a growing list of physiological and pathophysiological processes, coupled to a dysregulated immune response. This review focuses on new discoveries related to how ferroptotic cells and their spilled contents shape innate and adaptive immunity in health and disease. Understanding the immunological characteristics and activity of ferroptotic death not only illuminates an intersection between cell death and immunity but may also lead to the development of novel treatment approaches for immunopathological diseases.
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spelling pubmed-81269802021-12-07 Ferroptosis in infection, inflammation, and immunity Chen, Xin Kang, Rui Kroemer, Guido Tang, Daolin J Exp Med Review Ferroptosis is a type of regulated necrosis that is triggered by a combination of iron toxicity, lipid peroxidation, and plasma membrane damage. The upstream inducers of ferroptosis can be divided into two categories (biological versus chemical) and activate two major pathways (the extrinsic/transporter versus the intrinsic/enzymatic pathways). Excessive or deficient ferroptotic cell death is implicated in a growing list of physiological and pathophysiological processes, coupled to a dysregulated immune response. This review focuses on new discoveries related to how ferroptotic cells and their spilled contents shape innate and adaptive immunity in health and disease. Understanding the immunological characteristics and activity of ferroptotic death not only illuminates an intersection between cell death and immunity but may also lead to the development of novel treatment approaches for immunopathological diseases. Rockefeller University Press 2021-05-12 /pmc/articles/PMC8126980/ /pubmed/33978684 http://dx.doi.org/10.1084/jem.20210518 Text en © 2021 Chen et al. http://www.rupress.org/terms/https://creativecommons.org/licenses/by-nc-sa/4.0/This article is distributed under the terms of an Attribution–Noncommercial–Share Alike–No Mirror Sites license for the first six months after the publication date (see http://www.rupress.org/terms/). After six months it is available under a Creative Commons License (Attribution–Noncommercial–Share Alike 4.0 International license, as described at https://creativecommons.org/licenses/by-nc-sa/4.0/).
spellingShingle Review
Chen, Xin
Kang, Rui
Kroemer, Guido
Tang, Daolin
Ferroptosis in infection, inflammation, and immunity
title Ferroptosis in infection, inflammation, and immunity
title_full Ferroptosis in infection, inflammation, and immunity
title_fullStr Ferroptosis in infection, inflammation, and immunity
title_full_unstemmed Ferroptosis in infection, inflammation, and immunity
title_short Ferroptosis in infection, inflammation, and immunity
title_sort ferroptosis in infection, inflammation, and immunity
topic Review
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8126980/
https://www.ncbi.nlm.nih.gov/pubmed/33978684
http://dx.doi.org/10.1084/jem.20210518
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