Nuclear factor kappa-light-chain-enhancer of activated B cells and Transforming growth factor beta 1 signaling pathway proteins (NF-κB/TGF-β1 pathway)

The NF-κB/TGF-β1 pathway proteins represent a complex signaling axis involved in the regulation of inflammation, immune responses, and tissue remodeling. NF-κB is a primary mediator of inflammatory gene expression (UniProt P19838) [1], while TGF-β1 is a potent profibrotic cytokine that regulates cell growth and differentiation (UniProt P01137) [2]. The crosstalk between these two pathways is a critical driver of chronic diseases, particularly those involving fibrosis and cancer progression, where they cooperatively promote the epithelial-mesenchymal transition (EMT) [3]. In many pathological states, NF-κB activation can enhance TGF-β1 signaling, and conversely, TGF-β1 can trigger NF-κB through non-canonical pathways, creating a feed-forward loop that sustains chronic inflammation and tissue scarring. Therapeutic strategies targeting this axis include small molecule inhibitors of TGF-β receptors like Galunisertib, and multi-kinase or anti-fibrotic agents like Nintedanib and Pirfenidone [4, 5]. However, the pleiotropic nature of these proteins poses significant challenges, as systemic inhibition can lead to adverse effects such as impaired wound healing and immune dysfunction.

Other names

NF-kappaB/TGF-beta1 axisNF-kB/TGF-b1 crosstalkNF-kappaB and TGF-beta1 signaling components

Inhibition of TGF-β receptor kinase activity, inhibition of IKK-mediated phosphorylation of IκB, proteasomal degradation of NF-κB inhibitors, and neutralization of extracellular TGF-β ligands.