Pulmonary fibrosis is the end stage of numerous verbose parenchymal lung conditions. It's characterised by inordinate matrix conformation leading to destruction of the normal lung armature and eventually death. Despite an exponential increase in our understanding of potentially important intercessors and mechanisms, the delineation of primary pathways has proven to be fugitive. In this review vulnerability and pernicious agents, similar as contagions and gastro- oesophageal influx and their probable part in initiating complaint will be bandied. Farther motifs that are developed are seeker ancillary pathways, including vulnerable mechanisms, oxidative and endoplasmic reticulum stress, activation of the coagulation waterfall and the implicit part of stem cells. This review will try to give the anthology with an intertwined view on the current knowledge and attempts to give a road chart for unborn exploration. It's important to explore robust models of overall pathogenesis, coordinating a large number of clinical and scientific compliances. We believe that the integration of current data into a “big picture” overview of fibrogenesis is essential for the Development of effective antifibrotic strategies. The ultimate will presumably correspond of a combination of agents targeting a number of crucial pathways