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Cited by 566

The DOI matches its Crossref record; 137 of the 137 references it cites were found in a registry or an index.

Regulation of Nrf2 by Mitochondrial Reactive Oxygen Species in Physiology and Pathology

Open access
Kasai, Shuya, Shimizu, Sunao, Tatara, Yota, Mimura, Junsei, Itoh, Ken·2020·Biomolecules
DOI 10.3390/biom10020320
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Abstract

Reactive oxygen species (ROS) are byproducts of aerobic respiration and signaling molecules that control various cellular functions. Nrf2 governs the gene expression of endogenous antioxidant synthesis and ROS-eliminating enzymes in response to various electrophilic compounds that inactivate the negative regulator Keap1. Accumulating evidence has shown that mitochondrial ROS (mtROS) activate Nrf2, often mediated by certain protein kinases, and induce the expression of antioxidant genes and genes involved in mitochondrial quality/quantity control. Mild physiological stress, such as caloric restriction and exercise, elicits beneficial effects through a process known as “mitohormesis”. Exercise induces NOX4 expression in the heart, which activates Nrf2 and increases endurance capacity. Mice transiently depleted of SOD2 or overexpressing skeletal muscle-specific UCP1 exhibit Nrf2-mediated antioxidant gene expression and PGC1α-mediated mitochondrial biogenesis. ATF4 activation may induce a transcriptional program that enhances NADPH synthesis in the mitochondria and might cooperate with the Nrf2 antioxidant system. In response to severe oxidative stress, Nrf2 induces Klf9 expression, which represses mtROS-eliminating enzymes to enhance cell death. Nrf2 is inactivated in certain pathological conditions, such as diabetes, but Keap1 down-regulation or mtROS elimination rescues Nrf2 expression and improves the pathology. These reports aid us in understanding the roles of Nrf2 in pathophysiological alterations involving mtROS.

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Metadata

Authors
Kasai, S., Shimizu, S., Tatara, Y., Mimura, J., & Itoh, K.
Venue
Biomolecules
Publisher
MDPI AG
Published
2020-02-17
Volume
10
Issue
2
Pages
320
ISSN
2218-273X (ISSN-L)
DOI
10.3390/biom10020320
OpenAlex
W3006508170
Cited by
566
References
137
FWCI
17.77
Type
journal article
Language
en
Open access
gold

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CoChat. (2026). Citation check: Regulation of Nrf2 by Mitochondrial Reactive Oxygen Species in Physiology and Pathology. https://app.cochat.ai/papers/10.3390/biom10020320
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Kasai, S., Shimizu, S., Tatara, Y., Mimura, J., & Itoh, K. (2020). Regulation of Nrf2 by Mitochondrial Reactive Oxygen Species in Physiology and Pathology. Biomolecules. https://doi.org/10.3390/biom10020320

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Bibliographic data: Semantic Scholar, OpenAlex, Crossref.

Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).

Semantic Scholar’s data is described in: Kinney, R., et al. (2023). The Semantic Scholar Open Data Platform. arXiv:2301.10140.