NF-κB Signaling Pathway in Rheumatoid Arthritis: Mechanisms and Therapeutic Potential.

Autor: Liao H; The Second Clinical Medical College of Lanzhou University, Lanzhou, 730000, People's Republic of China.; Department of Rheumatology, Lanzhou University Second Hospital, Lanzhou, 730000, People's Republic of China., Zheng J; The Second Clinical Medical College of Lanzhou University, Lanzhou, 730000, People's Republic of China.; Department of Rheumatology, Lanzhou University Second Hospital, Lanzhou, 730000, People's Republic of China., Lu J; The Second Clinical Medical College of Lanzhou University, Lanzhou, 730000, People's Republic of China.; Department of Rheumatology, Lanzhou University Second Hospital, Lanzhou, 730000, People's Republic of China., Shen HL; The Second Clinical Medical College of Lanzhou University, Lanzhou, 730000, People's Republic of China. shenhl@lzu.edu.cn.; Department of Rheumatology, Lanzhou University Second Hospital, Lanzhou, 730000, People's Republic of China. shenhl@lzu.edu.cn.
Jazyk: angličtina
Zdroj: Molecular neurobiology [Mol Neurobiol] 2024 Nov 19. Date of Electronic Publication: 2024 Nov 19.
DOI: 10.1007/s12035-024-04634-2
Abstrakt: Rheumatoid arthritis (RA) is an autoimmune chronic inflammatory disease that imposes a heavy economic burden on patients and society. Bone and cartilage destruction is considered an important factor leading to RA, and inflammation, oxidative stress, and mitochondrial dysfunction are closely related to bone erosion and cartilage destruction in RA. Currently, there are limitations in the clinical treatment methods for RA, which urgently necessitates finding new effective treatments for patients. Nuclear transcription factor-κB (NF-κB) is a signaling transcription factor that is widely present in various cells. It plays an important role as a stress source in the cellular environment and regulates gene expression in processes such as immunity, inflammation, cell proliferation, and apoptosis. NF-κB has long been recognized as a pathogenic factor of RA, and its activation can exacerbate RA by promoting inflammation, oxidative stress, mitochondrial dysfunction, and bone destruction. Conversely, inhibiting the activity of the NF-κB pathway effectively inhibits these pathological processes, thereby alleviating RA. Therefore, NF-κB may be a potential therapeutic target for RA. This article describes the physiological structure of NF-κB and its important role in RA through the regulation of oxidative stress, inflammatory response, mitochondrial function, and bone destruction. Meanwhile, we also summarized the impact of NF-κB crosstalk with other signaling pathways on RA and the effect of related drugs or inhibitors targeting NF-κB on RA. The purpose of this article is to provide evidence for the role of NF-κB in RA and to emphasize its significant role in RA by elucidating the mechanisms, so as to provide a theoretical basis for targeting the NF-κB pathway as a treatment for RA.
Competing Interests: Declarations Ethics Approval and Consent to Participate Not applicable. Consent for Publication Not applicable. Competing Interests The authors declare no competing interests.
(© 2024. The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature.)
Databáze: MEDLINE
Externí odkaz: