Cited by 1,438Autophagy in Disease and TherapyRedox biology and oxidative stressMitochondrial Function and Pathology

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Autophagy, mitochondria and oxidative stress: cross-talk and redox signalling.

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Lee, Jisun, Giordano, Samantha, Zhang, Jianhua·2012·Biochemical Journal

DOI 10.1042/bj20111451PMC PMC3258656

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Abstract

Reactive oxygen and nitrogen species change cellular responses through diverse mechanisms that are now being defined. At low levels, they are signalling molecules, and at high levels, they damage organelles, particularly the mitochondria. Oxidative damage and the associated mitochondrial dysfunction may result in energy depletion, accumulation of cytotoxic mediators and cell death. Understanding the interface between stress adaptation and cell death then is important for understanding redox biology and disease pathogenesis. Recent studies have found that one major sensor of redox signalling at this switch in cellular responses is autophagy. Autophagic activities are mediated by a complex molecular machinery including more than 30 Atg (AuTophaGy-related) proteins and 50 lysosomal hydrolases. Autophagosomes form membrane structures, sequester damaged, oxidized or dysfunctional intracellular components and organelles, and direct them to the lysosomes for degradation. This autophagic process is the sole known mechanism for mitochondrial turnover. It has been speculated that dysfunction of autophagy may result in abnormal mitochondrial function and oxidative or nitrative stress. Emerging investigations have provided new understanding of how autophagy of mitochondria (also known as mitophagy) is controlled, and the impact of autophagic dysfunction on cellular oxidative stress. The present review highlights recent studies on redox signalling in the regulation of autophagy, in the context of the basic mechanisms of mitophagy. Furthermore, we discuss the impact of autophagy on mitochondrial function and accumulation of reactive species. This is particularly relevant to degenerative diseases in which oxidative stress occurs over time, and dysfunction in both the mitochondrial and autophagic pathways play a role.

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Authors: Lee, J., Giordano, S., & Zhang, J.
Affiliations: University of Alabama at Birmingham (US)
Corresponding author: Zhang, Jianhua
ORCID: Lee, Jisun
Zhang, Jianhua
Venue: Biochemical Journal
Publisher: Portland Press Ltd.
Published: 2011-12-21
Volume: 441
Issue: 2
Pages: 523-540
ISSN: 0264-6021 (ISSN-L)
1470-8728
DOI: 10.1042/bj20111451
PMC: PMC3258656
OpenAlex: W2124105006
Cited by: 1,438
References: 295
Citations by year: 2026: 45 · 2025: 58 · 2024: 65 · 2023: 68 · 2022: 98 · 2021: 99 · 2020: 110 · 2019: 116 · 2018: 143 · 2017: 119 · 2016: 104 · 2015: 115 · 2014: 118 · 2013: 118 · 2012: 62
FWCI: 11.18
Type: journal article
Language: en
Open access: hybrid
doi.org
Licence: cc-by-nc
creativecommons.org/licenses/by-nc/2.5/ (vor, 2773 d)
Locations: Biochemical Journal (publishedVersion, cc-by-nc)
Europe PMC (PubMed Central) (publishedVersion, cc-by-nc)
PubMed Central (publishedVersion, cc-by-nc)
PubMed (publishedVersion)
Funders: U.S. Department of Veterans Affairs
National Institute for Health and Care Research
National Institutes of Health (NS064090)
National Institute of Neurological Disorders and Stroke (R01NS064090)
Topics: Life Sciences › Biochemistry, Genetics and Molecular Biology › Cell Biology › Autophagy in Disease and Therapy
Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Redox biology and oxidative stress
Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Mitochondrial Function and Pathology
Keywords: autophagy, mitophagy, oxidative stress, redox signaling, reactive oxygen species, reactive nitrogen species, mitochondrial dysfunction, autophagy-related proteins, autophagosome formation, lysosomal degradation, mitochondrial turnover, cell death, degenerative diseases
MeSH terms: Protein Deglycase DJ-1, PTEN-Induced Putative Kinase, Animals, Autophagy, Cardiovascular Diseases, Humans, Hydrogen Peroxide, Lysosomes, Mitochondria, Neoplasms, Nitric Oxide, Oxidation-Reduction, Parkinson Disease, Protein Kinases, Transcription, Genetic, Signal Transduction, Oncogene Proteins, Reactive Oxygen Species, Oxidative Stress, Reactive Nitrogen Species, Intracellular Signaling Peptides and Proteins, TOR Serine-Threonine Kinases

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Autophagy, mitochondria and oxidative stress: cross-talk and redox signalling.

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