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dc.contributor.authorHuang, Michael L-H
dc.contributor.authorChiang, Shannon
dc.contributor.authorKalinowski, Danuta S
dc.contributor.authorBae, Dong-Hun
dc.contributor.authorSahni, Sumit
dc.contributor.authorRichardson, Des R
dc.date.accessioned2021-04-19T05:12:38Z
dc.date.available2021-04-19T05:12:38Z
dc.date.issued2019
dc.identifier.issn1942-0900en_US
dc.identifier.doi10.1155/2019/6392763en_US
dc.identifier.urihttp://hdl.handle.net/10072/403832
dc.description.abstractThe mitochondrion is an essential organelle important for the generation of ATP for cellular function. This is especially critical for cells with high energy demands, such as neurons for signal transmission and cardiomyocytes for the continuous mechanical work of the heart. However, deleterious reactive oxygen species are generated as a result of mitochondrial electron transport, requiring a rigorous activation of antioxidative defense in order to maintain homeostatic mitochondrial function. Indeed, recent studies have demonstrated that the dysregulation of antioxidant response leads to mitochondrial dysfunction in human degenerative diseases affecting the nervous system and the heart. In this review, we outline and discuss the mitochondrial and oxidative stress factors causing degenerative diseases, such as Alzheimer’s disease, Parkinson’s disease, amyotrophic lateral sclerosis, Huntington’s disease, and Friedreich’s ataxia. In particular, the pathological involvement of mitochondrial dysfunction in relation to oxidative stress, energy metabolism, mitochondrial dynamics, and cell death will be explored. Understanding the pathology and the development of these diseases has highlighted novel regulators in the homeostatic maintenance of mitochondria. Importantly, this offers potential therapeutic targets in the development of future treatments for these degenerative diseases.en_US
dc.description.peerreviewedYesen_US
dc.languageEnglishen_US
dc.publisherHindawien_US
dc.relation.ispartofjournalOxidative Medicine and Cellular Longevityen_US
dc.relation.ispartofvolume2019en_US
dc.subject.fieldofresearchMedical and Health Sciencesen_US
dc.subject.fieldofresearchcode11en_US
dc.subject.keywordsScience & Technologyen_US
dc.subject.keywordsLife Sciences & Biomedicineen_US
dc.subject.keywordsCell Biologyen_US
dc.subject.keywordsPRECURSOR PROTEINen_US
dc.subject.keywordsIRONen_US
dc.titleThe Role of the Antioxidant Response in Mitochondrial Dysfunction in Degenerative Diseases: Cross-Talk between Antioxidant Defense, Autophagy, and Apoptosisen_US
dc.typeJournal articleen_US
dc.type.descriptionC1 - Articlesen_US
dcterms.bibliographicCitationHuang, ML-H; Chiang, S; Kalinowski, DS; Bae, D-H; Sahni, S; Richardson, DR, The Role of the Antioxidant Response in Mitochondrial Dysfunction in Degenerative Diseases: Cross-Talk between Antioxidant Defense, Autophagy, and Apoptosis, Oxidative Medicine and Cellular Longevity, 2019, 2019en_US
dcterms.dateAccepted2019-02-11
dcterms.licensehttps://creativecommons.org/licenses/by/4.0/en_US
dc.date.updated2021-04-16T05:16:36Z
dc.description.versionVersion of Record (VoR)en_US
gro.rights.copyright© 2019 Michael L.-H. Huang et al. 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.en_US
gro.hasfulltextFull Text
gro.griffith.authorRichardson, Des R.


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