Ferroptosis as a Major Factor and Therapeutic Target for Neuroinflammation in Parkinson’s Disease

Mounting evidence suggests that ferroptosis is not just a consequence but also a fundamental contributor to the development and progression of Parkinson’s disease (PD). Ferroptosis is characterized as iron-dependent regulated cell death caused by excessive lipid peroxidation, leading to plasma membr...

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Autores principales:	Chih-Jan Ko, Shih-Ling Gao, Tsu-Kung Lin, Pei-Yi Chu, Hung-Yu Lin
Formato:	article
Lenguaje:	EN
Publicado:	MDPI AG 2021
Materias:	Parkinson’s disease ferroptosis neuroinflammation iron lipid peroxidation antioxidant defense Biology (General) QH301-705.5
Acceso en línea:	https://doaj.org/article/5028171a05484ed886d5fec872143624
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spelling	oai:doaj.org-article:5028171a05484ed886d5fec8721436242021-11-25T16:50:42ZFerroptosis as a Major Factor and Therapeutic Target for Neuroinflammation in Parkinson’s Disease10.3390/biomedicines91116792227-9059https://doaj.org/article/5028171a05484ed886d5fec8721436242021-11-01T00:00:00Zhttps://www.mdpi.com/2227-9059/9/11/1679https://doaj.org/toc/2227-9059Mounting evidence suggests that ferroptosis is not just a consequence but also a fundamental contributor to the development and progression of Parkinson’s disease (PD). Ferroptosis is characterized as iron-dependent regulated cell death caused by excessive lipid peroxidation, leading to plasma membrane rupture, release of damage-associated molecular patterns, and neuroinflammation. Due to the crucial role of intracellular iron in mediating the production of reactive oxygen species and the formation of lipid peroxides, ferroptosis is intimately controlled by regulators involved in many aspects of iron metabolism, including iron uptake, storage and export, and by pathways constituting the antioxidant systems. Translational and transcriptional regulation of iron homeostasis and redox status provide an integrated network to determine the sensitivity of ferroptosis. We herein review recent advances related to ferroptosis, ranging from fundamental mechanistic discoveries and cutting-edge preclinical animal studies, to clinical trials in PD and the regulation of neuroinflammation via ferroptosis pathways. Elucidating the roles of ferroptosis in the survival of dopaminergic neurons and microglial activity can enhance our understanding of the pathogenesis of PD and provide opportunities for the development of novel prevention and treatment strategies.Chih-Jan KoShih-Ling GaoTsu-Kung LinPei-Yi ChuHung-Yu LinMDPI AGarticleParkinson’s diseaseferroptosisneuroinflammationironlipid peroxidationantioxidant defenseBiology (General)QH301-705.5ENBiomedicines, Vol 9, Iss 1679, p 1679 (2021)
institution	DOAJ
collection	DOAJ
language	EN
topic	Parkinson’s disease ferroptosis neuroinflammation iron lipid peroxidation antioxidant defense Biology (General) QH301-705.5
spellingShingle	Parkinson’s disease ferroptosis neuroinflammation iron lipid peroxidation antioxidant defense Biology (General) QH301-705.5 Chih-Jan Ko Shih-Ling Gao Tsu-Kung Lin Pei-Yi Chu Hung-Yu Lin Ferroptosis as a Major Factor and Therapeutic Target for Neuroinflammation in Parkinson’s Disease
description	Mounting evidence suggests that ferroptosis is not just a consequence but also a fundamental contributor to the development and progression of Parkinson’s disease (PD). Ferroptosis is characterized as iron-dependent regulated cell death caused by excessive lipid peroxidation, leading to plasma membrane rupture, release of damage-associated molecular patterns, and neuroinflammation. Due to the crucial role of intracellular iron in mediating the production of reactive oxygen species and the formation of lipid peroxides, ferroptosis is intimately controlled by regulators involved in many aspects of iron metabolism, including iron uptake, storage and export, and by pathways constituting the antioxidant systems. Translational and transcriptional regulation of iron homeostasis and redox status provide an integrated network to determine the sensitivity of ferroptosis. We herein review recent advances related to ferroptosis, ranging from fundamental mechanistic discoveries and cutting-edge preclinical animal studies, to clinical trials in PD and the regulation of neuroinflammation via ferroptosis pathways. Elucidating the roles of ferroptosis in the survival of dopaminergic neurons and microglial activity can enhance our understanding of the pathogenesis of PD and provide opportunities for the development of novel prevention and treatment strategies.
format	article
author	Chih-Jan Ko Shih-Ling Gao Tsu-Kung Lin Pei-Yi Chu Hung-Yu Lin
author_facet	Chih-Jan Ko Shih-Ling Gao Tsu-Kung Lin Pei-Yi Chu Hung-Yu Lin
author_sort	Chih-Jan Ko
title	Ferroptosis as a Major Factor and Therapeutic Target for Neuroinflammation in Parkinson’s Disease
title_short	Ferroptosis as a Major Factor and Therapeutic Target for Neuroinflammation in Parkinson’s Disease
title_full	Ferroptosis as a Major Factor and Therapeutic Target for Neuroinflammation in Parkinson’s Disease
title_fullStr	Ferroptosis as a Major Factor and Therapeutic Target for Neuroinflammation in Parkinson’s Disease
title_full_unstemmed	Ferroptosis as a Major Factor and Therapeutic Target for Neuroinflammation in Parkinson’s Disease
title_sort	ferroptosis as a major factor and therapeutic target for neuroinflammation in parkinson’s disease
publisher	MDPI AG
publishDate	2021
url	https://doaj.org/article/5028171a05484ed886d5fec872143624
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Ferroptosis as a Major Factor and Therapeutic Target for Neuroinflammation in Parkinson’s Disease

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