Is Ferroptosis a Key Component of the Process Leading to Multiorgan Damage in COVID-19?

Even though COVID-19 is mostly well-known for affecting respiratory pathology, it can also result in several extrapulmonary manifestations, leading to multiorgan damage. A recent reported case of SARS-CoV-2 myocarditis with cardiogenic shock showed a signature of myocardial and kidney ferroptosis, a...

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Autores principales:	Anna Maria Fratta Pasini, Chiara Stranieri, Domenico Girelli, Fabiana Busti, Luciano Cominacini
Formato:	article
Lenguaje:	EN
Publicado:	MDPI AG 2021
Materias:	ferroptosis COVID-19 multiorgan damage iron GSH-GPX4 axis oxidative stress Therapeutics. Pharmacology RM1-950
Acceso en línea:	https://doaj.org/article/9c055f6238c048f28066693d2e186dc6
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spelling	oai:doaj.org-article:9c055f6238c048f28066693d2e186dc62021-11-25T16:25:53ZIs Ferroptosis a Key Component of the Process Leading to Multiorgan Damage in COVID-19?10.3390/antiox101116772076-3921https://doaj.org/article/9c055f6238c048f28066693d2e186dc62021-10-01T00:00:00Zhttps://www.mdpi.com/2076-3921/10/11/1677https://doaj.org/toc/2076-3921Even though COVID-19 is mostly well-known for affecting respiratory pathology, it can also result in several extrapulmonary manifestations, leading to multiorgan damage. A recent reported case of SARS-CoV-2 myocarditis with cardiogenic shock showed a signature of myocardial and kidney ferroptosis, a novel, iron-dependent programmed cell death. The term ferroptosis was coined in the last decade to describe the form of cell death induced by the small molecule erastin. As a specific inducer of ferroptosis, erastin inhibits cystine-glutamate antiporter system Xc-, blocking transportation into the cytoplasm of cystine, a precursor of glutathione (GSH) in exchange with glutamate and the consequent malfunction of GPX4. Ferroptosis is also promoted by intracellular iron overload and by the iron-dependent accumulation of polyunsaturated fatty acids (PUFA)-derived lipid peroxides. Since depletion of GSH, inactivation of GPX4, altered iron metabolism, and upregulation of PUFA peroxidation by reactive oxygen species are peculiar signs of COVID-19, there is the possibility that SARS-CoV-2 may trigger ferroptosis in the cells of multiple organs, thus contributing to multiorgan damage. Here, we review the molecular mechanisms of ferroptosis and its possible relationship with SARS-CoV-2 infection and multiorgan damage. Finally, we analyze the potential interventions that may combat ferroptosis and, therefore, reduce multiorgan damage.Anna Maria Fratta PasiniChiara StranieriDomenico GirelliFabiana BustiLuciano CominaciniMDPI AGarticleferroptosisCOVID-19multiorgan damageironGSH-GPX4 axisoxidative stressTherapeutics. PharmacologyRM1-950ENAntioxidants, Vol 10, Iss 1677, p 1677 (2021)
institution	DOAJ
collection	DOAJ
language	EN
topic	ferroptosis COVID-19 multiorgan damage iron GSH-GPX4 axis oxidative stress Therapeutics. Pharmacology RM1-950
spellingShingle	ferroptosis COVID-19 multiorgan damage iron GSH-GPX4 axis oxidative stress Therapeutics. Pharmacology RM1-950 Anna Maria Fratta Pasini Chiara Stranieri Domenico Girelli Fabiana Busti Luciano Cominacini Is Ferroptosis a Key Component of the Process Leading to Multiorgan Damage in COVID-19?
description	Even though COVID-19 is mostly well-known for affecting respiratory pathology, it can also result in several extrapulmonary manifestations, leading to multiorgan damage. A recent reported case of SARS-CoV-2 myocarditis with cardiogenic shock showed a signature of myocardial and kidney ferroptosis, a novel, iron-dependent programmed cell death. The term ferroptosis was coined in the last decade to describe the form of cell death induced by the small molecule erastin. As a specific inducer of ferroptosis, erastin inhibits cystine-glutamate antiporter system Xc-, blocking transportation into the cytoplasm of cystine, a precursor of glutathione (GSH) in exchange with glutamate and the consequent malfunction of GPX4. Ferroptosis is also promoted by intracellular iron overload and by the iron-dependent accumulation of polyunsaturated fatty acids (PUFA)-derived lipid peroxides. Since depletion of GSH, inactivation of GPX4, altered iron metabolism, and upregulation of PUFA peroxidation by reactive oxygen species are peculiar signs of COVID-19, there is the possibility that SARS-CoV-2 may trigger ferroptosis in the cells of multiple organs, thus contributing to multiorgan damage. Here, we review the molecular mechanisms of ferroptosis and its possible relationship with SARS-CoV-2 infection and multiorgan damage. Finally, we analyze the potential interventions that may combat ferroptosis and, therefore, reduce multiorgan damage.
format	article
author	Anna Maria Fratta Pasini Chiara Stranieri Domenico Girelli Fabiana Busti Luciano Cominacini
author_facet	Anna Maria Fratta Pasini Chiara Stranieri Domenico Girelli Fabiana Busti Luciano Cominacini
author_sort	Anna Maria Fratta Pasini
title	Is Ferroptosis a Key Component of the Process Leading to Multiorgan Damage in COVID-19?
title_short	Is Ferroptosis a Key Component of the Process Leading to Multiorgan Damage in COVID-19?
title_full	Is Ferroptosis a Key Component of the Process Leading to Multiorgan Damage in COVID-19?
title_fullStr	Is Ferroptosis a Key Component of the Process Leading to Multiorgan Damage in COVID-19?
title_full_unstemmed	Is Ferroptosis a Key Component of the Process Leading to Multiorgan Damage in COVID-19?
title_sort	is ferroptosis a key component of the process leading to multiorgan damage in covid-19?
publisher	MDPI AG
publishDate	2021
url	https://doaj.org/article/9c055f6238c048f28066693d2e186dc6
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Is Ferroptosis a Key Component of the Process Leading to Multiorgan Damage in COVID-19?

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