Fibrogenic and inflammatory signaling pathways

Fibrogenic and inflammatory signaling pathways represent a complex network of molecular interactions that drive tissue scarring and chronic immune responses (PubMed: 30272068). These pathways involve various cytokines (e.g., TGF-β, IL-6, TNF-α), growth factors (e.g., PDGF), and intracellular signaling cascades (e.g., SMAD, MAPK, JAK/STAT) that regulate the activation of fibroblasts and the recruitment of inflammatory cells (StatPearls: Fibrosis). In pathological states, persistent activation of these pathways leads to excessive deposition of extracellular matrix components, resulting in organ dysfunction and chronic diseases such as pulmonary fibrosis, cirrhosis, and chronic kidney disease (PubMed: 28438751). Therapeutic strategies often aim to inhibit specific nodes within these pathways, such as using Nintedanib to target tyrosine kinases or Pirfenidone to modulate TGF-β signaling, to halt or reverse disease progression (PubMed: 31067308). However, because these pathways are also essential for normal wound healing and immune defense, targeting them requires careful balance to avoid significant side effects like impaired healing or immunosuppression (PubMed: 25637160).

Other names

Pro-fibrotic signalingInflammatory cascadesFibrosis and inflammation pathwaysTissue remodeling pathways

Modulation of pro-inflammatory and pro-fibrotic mediators, including cytokines, growth factors, and their associated intracellular signaling transducers (e.g., SMADs, JAKs), to prevent myofibroblast activation and extracellular matrix deposition (PubMed: 30272068).