Inflammation and fibrosis pathways

Inflammation and fibrosis pathways represent a complex network of biological processes where chronic immune activation leads to excessive deposition of extracellular matrix components, such as collagen (StatPearls: NBK534744). This transition from acute inflammation to chronic fibrosis is a hallmark of many progressive diseases, including idiopathic pulmonary fibrosis, cirrhosis, and chronic kidney disease (NIH: PMC7019440). Key molecular drivers include cytokines like TGF-beta, TNF-alpha, and various interleukins, which activate fibroblasts into myofibroblasts (PubMed: 29241602). Therapeutic strategies often focus on blocking these signaling cascades to prevent organ dysfunction and tissue scarring. While many drugs target individual components of these pathways, such as tyrosine kinases or specific cytokine receptors, the redundancy and complexity of the network present significant challenges for achieving complete disease reversal (PubMed: 31034765).

Other names

Inflammatory-fibrotic axisChronic inflammation and tissue remodelingFibrogenesis signaling pathways

Inhibition of pro-inflammatory cytokines, blockade of growth factor receptor signaling, and modulation of fibroblast-to-myofibroblast transition.