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

Area of Science:

• Immunology
• Molecular Biology
• Rheumatology

Background:

• Rheumatoid arthritis (RA) is a chronic inflammatory disease causing significant economic burden.
• Bone and cartilage destruction are key features of RA, linked to inflammation, oxidative stress, and mitochondrial dysfunction.
• Current RA treatments have limitations, necessitating novel therapeutic approaches.

Purpose of the Study:

• To elucidate the role of nuclear transcription factor-κB (NF-κB) in rheumatoid arthritis (RA).
• To explore NF-κB as a potential therapeutic target for RA by examining its mechanisms in disease pathogenesis.
• To provide a theoretical basis for targeting the NF-κB pathway in RA treatment.

Main Methods:

• Review of NF-κB structure and function in cellular stress responses.
• Analysis of NF-κB's role in regulating inflammation, oxidative stress, mitochondrial dysfunction, and bone destruction in RA.
• Examination of NF-κB crosstalk with other signaling pathways in RA.
• Summary of drugs and inhibitors targeting the NF-κB pathway for RA treatment.

Main Results:

• NF-κB activation exacerbates RA by promoting inflammation, oxidative stress, mitochondrial dysfunction, and bone destruction.
• Inhibition of the NF-κB pathway effectively mitigates these pathological processes, alleviating RA.
• NF-κB plays a critical role in the pathogenesis of RA through multiple interconnected mechanisms.

Conclusions:

• NF-κB is a significant pathogenic factor in RA.
• Targeting the NF-κB pathway presents a viable therapeutic strategy for managing RA.
• Further research into NF-κB inhibitors could lead to improved RA treatments.