Inflammatory mediators in various molecular pathways involved in the development of pulmonary fibrosis.

Idiopathic pulmonary fibrosis (IPF) is a type of interstitial lung disease (ILD) that is marked by scarring of lung tissue, ultimately leading to respiratory failure. The survival rate of IPF is disappointing and to date demonstrates a clinical quandary. The exact etiology of the disease remains under discussion. According to the recent hypothesis, inflammatory mediators cause severe damage to the alveolar epithelium leading to the impairment of the alveolar structure. The role of inflammation in the development of the IPF has been controversial for years. There are two schools of thought regarding the role of inflammation. One group of researchers claims that cell death and fibroblast dysfunction are the primary causes and inflammation is just a secondary cause of IPF. The other group claims inflammation to be the primary cause. Studies using human subjects have also reported inflammation as a critical element in IPF. Inflammatory cytokinesserve amajor rolein commencing theinflammatoryresponse in the lungs. Several cytokines are reported to be involved in different molecular mechanisms underlying IPF, someof which alsocontribute additionally by acting as growth factors. The present review addressed to explore the contribution of various inflammatory cytokines, growth factors, and various other inflammatory molecules activating the major molecular pathways involved during the development of IPF.