Pro-inflammatory and Fibrotic Signaling Pathways

Pro-inflammatory and Fibrotic Signaling Pathways" refers to a network of interconnected molecular cascades that govern both inflammatory responses and tissue fibrosis. These pathways include classical inflammation mediators (such as NF-κB, JAK-STAT, and MAPK) and pro-fibrotic effectors (such as TGF-β/Smad, PI3K/AKT, and JNK), which collectively regulate processes like immune cell activation, cytokine secretion, fibroblast-to-myofibroblast transition, and extracellular matrix deposition[1][2][3][4][5][6][7]. Key molecules implicated include cytokines (e.g., IL-1β, IL-6, TNF-α), growth factors (e.g., TGF-β, PDGF), and downstream intracellular pathways (including Smad proteins, AKT, and AP-1). The activation and interaction of these pathways drive chronic inflammation and the development of fibrosis in various tissues, underlying diseases such as idiopathic pulmonary fibrosis, chronic liver and kidney disease, and some cancers. Because this is not a singular molecular entity but an umbrella term for multiple pathways and mediators, it is not considered a canonical drug target[1][2][3][4][5][6][7].

Other names

pro-inflammatory signaling pathwayspro-fibrotic signaling pathwaysinflammatory and fibrotic pathways