MCTR1 Intervention Reverses Experimental Lung Fibrosis in Mice

Area of Science:

• Pulmonary Medicine
• Inflammation Research
• Drug Discovery

Background:

• Pulmonary fibrosis (PF) is a progressive, lethal lung disease with limited therapeutic options.
• Maresin conjugates in tissue regeneration 1 (MCTR1), a macrophage-derived mediator, promotes inflammation resolution.
• The therapeutic potential of MCTR1 in PF remains unexplored.

Purpose of the Study:

• To investigate the efficacy of MCTR1 in a mouse model of bleomycin-induced pulmonary fibrosis.
• To determine if MCTR1 can attenuate lung inflammation, fibrosis, and improve lung function.

Main Methods:

• A pulmonary fibrosis model was induced using bleomycin (BLM) in mice.
• MCTR1 treatment was administered post-induction, with daily body weight monitoring and survival analysis.
• Histological, ultrastructural, and molecular analyses (ELISA, q-PCR, Western blot) assessed inflammation, fibrosis, epithelial-to-mesenchymal transition (EMT), and lung function.

Main Results:

• MCTR1 intervention significantly attenuated BLM-induced lung inflammation and fibrotic responses.
• MCTR1 protected against BLM-induced epithelial cell damage and reversed EMT.
• Post-treatment with MCTR1 improved lung function and significantly enhanced survival rates.

Conclusions:

• MCTR1 effectively mitigated inflammation and fibrosis in a mouse model of pulmonary fibrosis.
• MCTR1 demonstrates potential as a novel therapeutic strategy for treating fibrosis-related lung diseases.