Abstract: Regardless of the etiology of pulmonary fibrosis, Myofibroblasts (MFs) play an important role in the progression of chronic inflammation and fibrosis. Persistent tissue damage is critical in initiating and perpetuating the different sources of MF precursor cells into myofibroblasts that share peculiar traits and phenotypic responses, including the ability to proliferate, migration, produce extracellular matrix components and contribute to modulation of inflammatory response and tissue angiogenesis. The activation of myofibroblast cells involves the activation of TGF -β, PDGF, CTGF and other cytokines, as well as the involvement of Wnt β-catenin signaling pathway, tissue rigidity and mechanical stretching, and microRNA.

Key words: pulmonary fibrosis, myofibroblast, activation, mechanism