NF-κB and Its Role in Health and Disease

Dear Colleagues,

Nuclear factor-kappa B (NF-κB) is a transcription factor that plays a pivotal role in immune responses, inflammation, cell survival, and various physiological processes. The activity of NF-κB is tightly regulated and essential for maintaining homeostasis in the body. However, the dysregulation of NF-κB signaling has been implicated in the pathogenesis of numerous diseases.

In normal physiological conditions, NF-κB is maintained in an inactive state in the cytoplasm through its interaction with inhibitory proteins called IκBs (inhibitor of κB). Upon activation by various stimuli, such as pro-inflammatory cytokines or pathogens, the IκB proteins are phosphorylated and degraded, allowing NF-κB to translocate into the nucleus. Once in the nucleus, NF-κB binds to specific DNA sequences, known as κB sites, and regulates the transcription of target genes, which are involved in inflammation, chemokines, cell survival, and so on. These functions are important for maintaining healthy immune homeostasis, wound healing, and tissue development.

However, aberrant NF-κB activation is implicated in the pathogenesis of numerous diseases such as neurodegenerative disorders, autoimmune diseases, and metabolic disorders. In these diseases, abnormal NF-κB activation contributes to tissue damage, oxidative stress, and chronic inflammation.

Given the prominent role of NF-κB in disease pathogenesis, targeting NF-κB signaling has emerged as a therapeutic strategy. The goal is to restore the balance of NF-κB activation, alleviate inflammation, and potentially mitigate the progression of various diseases.

There are several unsolved issues in NF-κB-related diseases, such as the specificity of targeting NF-κB, as it is involved in numerous cellular processes and regulates a wide range of genes. Additionally, achieving the selective inhibition of pathological NF-κB activity without disrupting its physiological functions remains a challenge. The complexity of NF-κB signaling networks and the crosstalk with other pathways make it challenging to unravel the specific contributions of NF-κB in disease pathogenesis. Therefore, this Special Issue provides a platform where you can publish your research on any aspect of NF-κB-related health and diseases, including the pathophysiologic mechanisms, diagnosis, and treatment of inflammatory disease, or experimental, translational, and clinical research. We accept reviews, short communications, methodology papers, and full-size research papers with a focus on understanding the mechanisms of NF-κB signaling in health and diseases and provide valuable insights for developing targeted therapies and interventions to manage inflammatory and immune-related disorders.

Dr. Jun Yan
Guest Editor

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• NF-κB
• κB
• IKKs
• inflammation
• pro-inflammation
• immune system
• disease
• biomarker
• gene