Context:Oestrogen deficiency is linked with pulmonary fibrosis. Additionally, it may lead to over-acti-vation of the renin-angiotensin system (RAS), which worsens lung fibrosis.Objective:The present study aims to investigate the role of RAS on lung fibrosis associated with oes-trogen deficiency in ovariectomised rats.Materials and methods:Serum 17b-oestradiol (E2), arterial blood gases, plasma angiotensin II levels,lung tissue hydroxyproline content, and transforming growth factor beta 1 (TGF-b1) concentration, themRNA expression of angiotensin type 1 receptor (AT1R), and angiotensin-converting enzyme (ACE1)were evaluated. Moreover, lung tissues were examined by histopathology and immunohistochemistry.Results:Hydroxyproline content, TGF-b1 concentration, plasma angiotensin II, the relative mRNAexpression of ACE1, and AT1R is found to increase in ovariectomised rats. The mentioned changes canbe largely rescued by administration of RAS blockers.Conclusion:Oestrogen deficiency activates RAS, which consequently increases the expression ofpro-fibrotic factors and stimulates the fibrotic cascade causing lung fibrosis