NF-κB in oxidative stress
Open accessAbstract
The transcription factor nuclear factor-κB (NF-κB) modulates gene expression in diverse cellular processes such as innate immune response, embryogenesis and organ development, cell proliferation and apoptosis, and stress responses to a variety of noxious stimuli. When cellular production of reactive oxygen species (ROS) overwhelms its antioxidant capacity, it leads to a state of oxidative stress, which in turn contributes to the pathogenesis of several human diseases. Different models of oxidative stress have been studied to elucidate the effects of oxidant stress on NF-κB related activities. ROS can both activate and repress NF-κB signaling in a phase and context dependent manner. The NF-κB pathway can have both anti- and pro-oxidant roles in the setting of oxidative stress. In this review, we focus on role of oxidative stress on different mediators of the NF-κB pathway, and the role of NF-κB activation in the modulation of oxidative stress. A greater understanding of the complex interplay between the NF-κB signaling and oxidative stress may lead to the development of therapeutic strategies for the treatment of a myriad of human diseases for which oxidative stress has an etiologic role.
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ROS can either activate or suppress NF-kB signaling involved in the control of embryogenesis, cell proliferation and death, and responses to stress stimuli.
“These data show that ROS can either activate or suppress the NF-kB signaling involved in the control of several important cellular processes, such as embryogenesis and cell proliferation and death, and the responses to a variety of stress stimuli37.”
From ROS in cancer therapy: the bright side of the moon (2020) · cites this paper as [37]
Proinflammatory master gene NF-κB is a redox sensitive transcription factor.
“For instance, proinflammatory master gene NF-κB is a redox sensitive transcription factor (53).”
From Melatonin Attenuates LPS-Induced Acute Depressive-Like Behaviors and Microglial NLRP3 Inflammasome Activation Through the SIRT1/Nrf2 Pathway (2019) · cites this paper as [53]
NF-κB activates genes of pro-oxidant enzymes such as NADPH oxidases and COX2.
“Conversely, NF-κB activates genes of pro-oxidant enzymes such as NADPH oxidases and COX2 (53).”
From Melatonin Attenuates LPS-Induced Acute Depressive-Like Behaviors and Microglial NLRP3 Inflammasome Activation Through the SIRT1/Nrf2 Pathway (2019) · cites this paper as [53]
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- Authors
- Lingappan, K.
- Affiliations
- Baylor College of Medicine (US)
- Corresponding author
- Lingappan, Krithika
- ORCID
- Lingappan, Krithika
- Venue
- Current Opinion in Toxicology
- Publisher
- Elsevier BV
- Published
- 2018-02
- Volume
- 7
- Pages
- 81-86
- ISSN
- 2468-2020 (ISSN-L)
- PMC
- PMC5978768
- OpenAlex
- W2767765728
- Cited by
- 1,051
- References
- 55
- Citations by year
- 2026: 147 · 2025: 231 · 2024: 180 · 2023: 133 · 2022: 139 · 2021: 114 · 2020: 75 · 2019: 26 · 2018: 4 · 2014: 1
- FWCI
- 2.92
- Type
- journal article
- Language
- en
- Open access
- green
- europepmc.org
- Locations
- Current Opinion in Toxicology (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Heart, Lung, and Blood Institute (K08HL127103)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › NF-κB Signaling Pathways
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Redox biology and oxidative stress
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Genomics, phytochemicals, and oxidative stress
- Keywords
- NF-κB signaling, oxidative stress, reactive oxygen species, antioxidant capacity, NF-κB activation, stress response, pathogenesis, treatment options
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