Pro-fibrotic and pro-inflammatory pathways

Pro-fibrotic and pro-inflammatory pathways represent a complex network of signaling cascades that drive tissue scarring and chronic inflammation (Meng et al., Nat Rev Nephrol, 2016). These pathways are typically initiated by tissue injury or persistent immune activation, leading to the recruitment of inflammatory cells and the activation of fibroblasts into myofibroblasts (Brenner et al., Nat Rev Rheumatol, 2014). Key molecular drivers include cytokines like tumor necrosis factor-alpha (TNF-alpha) and interleukins, as well as growth factors such as transforming growth factor-beta (TGF-beta). While these processes are essential for normal wound healing, their dysregulation leads to chronic diseases such as pulmonary fibrosis, cirrhosis, and rheumatoid arthritis (Wynn, J Clin Invest, 2007). Therapeutic strategies often focus on inhibiting specific receptors or kinases within these pathways, such as the multi-kinase inhibitor nintedanib or the anti-fibrotic agent pirfenidone, to halt disease progression (Richeldi et al., NEJM, 2014). Because these pathways are highly redundant and pleiotropic, therapeutic development often faces challenges related to systemic toxicity and off-target effects.

Other names

Fibrotic signaling cascadesInflammatory signaling pathwaysPro-fibrotic and pro-inflammatory signaling network

Modulation of signaling cascades through the inhibition of specific ligands, receptors, or downstream signaling molecules (e.g., kinases) to reduce inflammatory cell infiltration and fibroblast activation (Meng et al., Nat Rev Nephrol, 2016).