LGMN promotes crosstalk between macrophages and fibroblasts in pulmonary fibrosis: a potential therapeutic target

Background: Macrophages play a crucial role in the progression of idiopathic pulmonary fibrosis (IPF). This study aims to identify a predictive signature based on macrophage-related genes to forecast patient prognosis and uncover potential therapeutic targets for IPF. Methods: experiments. Results: experiments demonstrated elevated levels of LGMN in M2 macrophages, co-localizing with CD206 in fibrotic lung tissue. Treatment with RR-11a, a LGMN inhibitor, reduced TGF-β1 secretion from M2 macrophages, thereby diminishing communication between macrophages and fibroblasts and alleviating bleomycin-induced pulmonary fibrosis in mice. Conclusions: Our research establishes a gene signature associated with MDMs, which may aid clinicians in the personalized management of IPF. Additionally, we identify LGMN as a promoter of interaction between M2 macrophages and fibroblasts, suggesting its potential as a therapeutic target for IPF treatment.