Cited by 288Genomics, phytochemicals, and oxidative stressNuclear Receptors and SignalingEndoplasmic Reticulum Stress and Disease

Oxidative damage and the Nrf2-ARE pathway in neurodegenerative diseases

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Gan, Li, Johnson, Jeffrey A.·2014·Biochimica et Biophysica Acta (BBA) - Molecular Basis of Disease

Abstract

Oxidative damage contributes to pathogenesis in many neurodegenerative diseases. As the indicator and regulator of oxidative stress, the Nrf2-ARE pathway has been shown dynamic changes and examined for its neuroprotective role in many cases. In this review, we summarize the progress of the Nrf2-ARE pathway in combating toxicity induced from typical misfolded protein aggregates in neurodegenerative diseases, and specifically the effects on the clearance of protein aggregates.

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Authors
Gan, L., & Johnson, J. A.
Affiliations
University of Wisconsin–Madison (US)
Corresponding author
Johnson, Jeffrey A.
Venue
Biochimica et Biophysica Acta (BBA) - Molecular Basis of Disease
Publisher
Elsevier BV
Published
2014-08
Volume
1842
Issue
8
Pages
1208-1218
ISSN
0925-4439 (ISSN-L)
OpenAlex
W2011199467
Cited by
288
References
166
Citations by year
2026: 13 · 2025: 16 · 2024: 22 · 2023: 24 · 2022: 26 · 2021: 28 · 2020: 19 · 2019: 22 · 2018: 19 · 2017: 35 · 2016: 25 · 2015: 26 · 2014: 13
FWCI
3.11
Type
journal article
Language
en
Open access
Locations
  • Biochimica et Biophysica Acta (BBA) - Molecular Basis of Disease (publishedVersion)
  • PubMed (publishedVersion)
Funders
National Institute of Environmental Health Science (ES10042, ES08089)
Topics
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Genomics, phytochemicals, and oxidative stress
  • Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Nuclear Receptors and Signaling
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Cell Biology › Endoplasmic Reticulum Stress and Disease
Keywords
Nrf2/ARE pathway, oxidative stress, neurodegenerative diseases, protein aggregation, misfolded proteins, neuroprotection, protein aggregate clearance, oxidative damage
MeSH terms
Animals, Humans, Signal Transduction, Oxidative Stress, Neuroprotective Agents, Neurodegenerative Diseases, NF-E2-Related Factor 2, Antioxidant Response Elements

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