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While Metformin inhibits complex 1 of the respiratory chain in the mitochondria leading to an increase in adenosine monophosphate (AMP) and activation of AMP-activated protein kinase (AMPK), which in turn inhibits hepatic gluconeogenesis, the concentration of Metformin needed to achieve such effects in humans is supra-therapeutic (71, 72)

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They demonstrated that the ECM supports both epithelial cells and fibroblasts, with TGF- contributing to the remodelling of the ECM, indicating its potential as a therapeutic target

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