Pulmonary fibrosis (PF) is an irreversible, progressive, fatal lung disease where chronic inflammation triggers and initiates the development of a fibrotic condition in lung tissue. Abnormal repair of lung tissue is a serious pathological condition in the case of IPF. The FDA recently approved pirfenidone and nintedanib for the treatment of IPF. However, both compounds have tolerability problems; their efficacy is limited, with many patients progressing to end stage disease. Therefore, it is important to explore novel therapeutic targets and develop potential drugs for IPF. The endocannabinoid system (ECS) consists of endocannabinoids, cannabinoid receptors, and related enzymes. The role of cannabinoid receptors in the nervous system is established, but a few recent studies suggest that the ECS with immunomodulatory functions serves as a target in treating inflammatory and fibrotic diseases. For example, in bleomycin (BLM)induced experimental skin fibrosis, the CB2R agonist inhibited collagen synthesis and delayed ECM deposition as well as prevented fibrotic progression in vitro and in vivo. In this review article, we summarize several fruitful studies that account for the therapeutic targeting of the endocannabinoid system in the context of PF. Various cannabinoid type 2 receptor (CB2R) agonists such as AM1241, JWH133, WIN 55212–2, etc. show promising results in the case of fibrosis. Icariin (ICA), a natural compound, exerts a potential therapeutic effect in experimental PF. URB937, an inhibitor of fatty acid amide hydrolase, attenuates radiation induced lung fibrosis. The hybrid CB1R/iNOS inhibitor has greater anti-fibrotic efficacy than inhibition of CB1R alone, thus making it a viable candidate for future translational studies in IPF.