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Fig. 7 | European Journal of Medical Research

Fig. 7

From: Amifostine ameliorates bleomycin-induced murine pulmonary fibrosis via NAD+/SIRT1/AMPK pathway-mediated effects on mitochondrial function and cellular metabolism

Fig. 7

Schematic mechanism for the therapeutic effects of amifostine on IPF. The Profibrotic stimuli bleomycin and TGF-β1 induce comprehensive mitochondrial dysfunction due to increased ROS production, loss of mitochondrial membrane potential, and changes in the metabolite profile. Amifostine inhibits excessive mitochondrial ROS production, restores the mitochondrial membrane potential, and maintains homeostasis of mitochondrial metabolism. Restored NAD+ activates SIRT1 and its downstream kinase AMPK, which in turn inhibits the development of pulmonary fibrosis

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European Journal of Medical Research

ISSN: 2047-783X

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