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Cited by 8,791NF-κB Signaling PathwaysImmune Response and InflammationSignaling Pathways in Disease

NF-κB signaling in inflammation

Open access
Liu, Ting, Zhang, Lingyun, Joo, Donghyun, Sun, Shao-Cong·2017·Signal Transduction and Targeted Therapy
DOI 10.1038/sigtrans.2017.23PMC PMC5661633
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Abstract

The transcription factor NF-κB regulates multiple aspects of innate and adaptive immune functions and serves as a pivotal mediator of inflammatory responses. NF-κB induces the expression of various pro-inflammatory genes, including those encoding cytokines and chemokines, and also participates in inflammasome regulation. In addition, NF-κB plays a critical role in regulating the survival, activation and differentiation of innate immune cells and inflammatory T cells. Consequently, deregulated NF-κB activation contributes to the pathogenic processes of various inflammatory diseases. In this review, we will discuss the activation and function of NF-κB in association with inflammatory diseases and highlight the development of therapeutic strategies based on NF-κB inhibition.

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Crossref · 10.1038/sigtrans.2017.23

Cites

140 of 140 references verified0 citation errors · 0 not checkable

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  • NF-κB p65 and p38 MAPK signaling pathways are key regulators of inflammation and pro-inflammatory responses.

    “Both signaling pathways are key regulators of inflammation and pro-inflammatory responses, which are considered targets for developing anti-inflammatory therapeutic agents [23–26].”

    From The potential of GHK as an anti-aging peptide (2020) · cites this paper as [23]

    The Introduction identifies p65 (RelA) as an NF-κB family member, and the section on pro-inflammatory gene induction calls NF-κB a central mediator of that process. The Concluding Remarks describe NF-κB signaling as a potential anti-inflammatory therapeutic target. The passages found do not support the corresponding claim about p38 MAPK. (LLM, conf=0.88)

    Experimental — accuracy not yet measured

  • Activation of Akt leads to phosphorylation of numerous target proteins that affect gene transcription, one of which is NF-kB, an important mediator of inflammation.

    “Activation of Akt leads to phosphorylation of numerous target proteins that in turn affect gene transcription, one of which is NF-kB, an important mediator of inflammation [87].”

    From Microglial function, INPP5D/SHIP1 signaling, and NLRP3 inflammasome activation: implications for Alzheimer’s disease (2023) · cites this paper as [87]

    The Introduction (page unavailable) identifies NF-κB as a transcription factor involved in inflammatory responses. It describes IKK-mediated phosphorylation of IκBα as a route to NF-κB activation, but does not support the claim that activated Akt phosphorylates NF-κB or numerous transcription-related targets (searched: Akt phosphorylation, Akt kinase). (LLM, conf=0.87)

    Experimental — accuracy not yet measured

  • Activated Akt stimulates IKKα of the IKK kinase complex, leading to degradation of IkB.

    “Activated Akt stimulates IKKα of the IKK kinase complex, which leads to the degradation of the NF-kB complex inhibitory protein IkB.”

    From Microglial function, INPP5D/SHIP1 signaling, and NLRP3 inflammasome activation: implications for Alzheimer’s disease (2023) · cites this paper as [87]

    The Introduction (page unavailable) identifies IKKα as a subunit of the IKK complex and says activated IKK triggers IκBα degradation. It does not say that activated Akt stimulates IKKα; a search for Akt found no passage supporting that step. (LLM, conf=0.88)

    Experimental — accuracy not yet measured

  • NF-κB activation promotes transcription of the nod-like receptor family pyrin domain, initiating inflammasome activation.

    “NF-κB activation also promotes the transcription of the nod-like receptor family pyrin domain, initiating inflammasome activation53.”

    From Air Pollution and Skin Diseases (2025) · cites this paper as [53]

  • NF-κB is a transcription factor that regulates the immune response and inflammatory response, and regulates gene expression in response to multiple stimuli.

    “NF-κB is a transcription factor that regulates the immune response and inflammatory response, and regulates gene expression in response to multiple stimuli [57]”

    From Picroside II suppresses chondrocyte pyroptosis through MAPK/NF-κB/NLRP3 signaling pathway alleviates osteoarthritis (2024) · cites this paper as [57]

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Authors
Liu, T., Zhang, L., Joo, D., & Sun, S.-C.
Affiliations
The University of Texas MD Anderson Cancer Center (US)
Corresponding author
Sun, Shao-Cong
ORCID
Venue
Signal Transduction and Targeted Therapy
Publisher
Springer Science and Business Media LLC
Published
2017-07-14
Volume
2
Issue
1
ISSN
2059-3635 (ISSN-L)
DOI
10.1038/sigtrans.2017.23
PMC
PMC5661633
OpenAlex
W2735527928
Semantic Scholar
dee351f96a0a7b9da6ce156c06c6b8654d8a09ec
Cited by
8,791
References
140
Citations by year
2026: 1021 · 2025: 1440 · 2024: 1462 · 2023: 1279 · 2022: 1237 · 2021: 1041 · 2020: 825 · 2019: 376 · 2018: 94 · 2017: 1 · 2014: 1
FWCI
119.12
Type
journal article
Language
en
Open access
Licence
Locations
  • Signal Transduction and Targeted Therapy (publishedVersion, cc-by)
  • Europe PMC (PubMed Central) (publishedVersion, cc-by)
  • PubMed Central (publishedVersion, cc-by)
  • PubMed (publishedVersion)
Funders
  • National Institutes of Health (AI064639)
  • National Institute of General Medical Sciences (R01GM084459)
  • National Institute of Allergy and Infectious Diseases (R01AI057555, R37AI064639, R01AI064639, R01AI104519)
Topics
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › NF-κB Signaling Pathways
  • Life Sciences › Immunology and Microbiology › Immunology › Immune Response and Inflammation
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Signaling Pathways in Disease
Keywords
NF-κB signaling, inflammation, inflammatory diseases, innate immunity, adaptive immunity, cytokines, chemokines, inflammasome, immune cell differentiation, NF-κB inhibition, treatment options

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