<p>Pulmonary<?tk 4?> fibrosis is a serious threat to global health, especially in after math of covid-19 infection, eventually results in fibrotic remodeling and organ damage. This SARS-CoV 2 induced fibrosis initiates cascade of proinflammatory responses such as cytokine release. EMT (Epithelial-mesenchymal transition) is a central event in post COVID 19 pulmonary fibrosis which is characterized by the accumulation of stimulated fibroblast and myoblast, finally epithelial morphology changed to mesenchymal traits. This transformation is marked by the loss of intercellular adhesion and polarity. A study of SARS-CoV 2 pathogenesis and EMT can provide insights to pulmonary fibrosis. Hence identification of biomarkers of EMT activation helps early diagnosis and determination of therapeutic approaches against pathogenesis. This review focusing on the mechanism of post-covid 19 pulmonary fibrosis through EMT with a special importance to TGF-β/Smad, NF-κB pathways and oxidative stress. Previous studies marked the EMT induced fibronectin, collagen deposition that can potentially disrupt lung structure and its function. SARS CoV 2 infection can trigger Hyper activation of profibrotic pathways like TGF-β/Smad, NF-κB pathways that maintain EMT via downregulation of E-Cadherin and upregulation of vimentin, fibronectin and α-SMA. SARS-CoV spike-protein binds to AEC-2 cells initiates cytokine storm followed by amplified NF-κB pathway, and oxidative stress. Elevated activation of this pathway increases Snail, Slug, Twist expression that leads to EMT. Moreover, increased ROS production creates fibrotic environment in lung. This review examined the mechanism behind the pulmonary fibrosis by analyzing interplay between the SARS-CoV 2 infection and EMT, providing effective therapeutic strategies to prevent EMT.</p> Graphical abstract <p></p>