Metformin as Potential Treatment for Pulmonary Fibrosis Through AMPK Activation and Fibroblast Reprogramming

Pulmonary Fibrosis (PF) is a subtype of ILD (interstitial lung disease) characterized by a chronic and progressive disease causing lung tissue to become thick and stiff due to the overactivation of fibroblasts in the lung tissues. Relating to pulmonary fibrosis, metformin has shown to have antifibrotic effects and in the best cases, a reversal of existing fibrosis unlike any other approved treatments for PF. The aim of study was to conclude how metformin could work to reverse fibrosis in PF through existing datasets. Analyzing miRNAs heavily upregulated in Systematic-Sclerosis associated ILD (SSc-ILD) patents in data processing programs like DAVID and Enrichr had revealed significant activity in the signalling pathway of AMPK enzymes. Metformin revealed a formidable AMPK activator. Upregulation of the AMPK enzyme has shown the lead the the decrease in fibroblast differential into myofibroblast, indicating a decrease in fibrosis. This paper explores the molecular mechanism and potentials of metformin as a drug for pulmonary fibrosis patients. Future research could build on this by testing metformin’s antifibrotic effects in clinical trials. This work also points to AMPK as a promising target for treating fibrosis more broadly in other organs as well.