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

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

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

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.

The claims and statistics of this paper haven’t been checked yet.

Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.

A few free checks a day · papers already verified open instantly · results are public

Integrity signals

Registry

Crossref · 10.1042/bj20111451

Cites

295 of 295 references verified0 citation errors · 0 not checkable

Statistics

Claims the paper makes

The claims and statistics of this paper haven’t been checked yet.

Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.

A few free checks a day · papers already verified open instantly · results are public

Claims other papers make about this one

Each is checked against this paper’s own text: does it say what the citing paper says it does?

Self-check

Percentages, sums and reported differences re-computed from the paper’s own numbers.

The self-check needs the paper’s full text.

Cites

2 retracted

Flagged first, then by citations

Cited by

Sorted by citations

Authors
Lee, J., Giordano, S., & Zhang, J.
Affiliations
University of Alabama at Birmingham (US)
Corresponding author
Zhang, Jianhua
Venue
Biochemical Journal
Published
2011-12-21
Volume
441
Issue
2
Pages
523-540
ISSN
  • 0264-6021 (ISSN-L)
  • 1470-8728
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
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
  • Health Sciences › Medicine › Epidemiology › 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

About these checks

Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.

Statistics and arithmetic are recomputed, not judged.

Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.

What counts as a claim ›How we measure confidence ›How we check this ›

Are you an author, or do you see a problem with this page? Request a review