Metformin reverses established lung fibrosis in a bleomycin model.

ABSTRACT: Fibrosis is a pathological result of a dysfunctional repair response to tissue injury and occurs in a number of organs, including the lungs¹. Cellular metabolism regulates tissue repair and remodelling responses to injury^2-4. AMPK is a critical sensor of cellular bioenergetics and controls the switch from anabolic to catabolic metabolism⁵. However, the role of AMPK in fibrosis is not well understood. Here, we demonstrate that in humans with idiopathic pulmonary fibrosis (IPF) and in an experimental mouse model of lung fibrosis, AMPK activity is lower in fibrotic regions associated with metabolically active and apoptosis-resistant myofibroblasts. Pharmacological activation of AMPK in myofibroblasts from lungs of humans with IPF display lower fibrotic activit

SUBMITTER: Rangarajan S 

PROVIDER: S-EPMC6081262 | biostudies-literature | 2018 Aug

REPOSITORIES: biostudies-literature