Fatty acid synthase is required for profibrotic TGF‐β signaling

What is it about?

Idiopathic Pulmonary Fibrosis (IPF) is a rapidly progressing disease whereby patients typically die within three years of diagnosis from lung failure. Currently there is no clinically effective treatment. The fibrotic environment represents the concerted action of a number of blood-borne or locally elaborated cytokines and growth factors, of which Transforming Growth Factor beta (TGF-β) is chief among them. As TGF-β is the primary cytokine mediating the development and/or progression of organ fibrosis, identifying the operative targets/mechanisms mediating its actions is critical if we hope to identify effective therapeutic strategies. To that end, since alterations in cellular metabolism are known to play critical roles in a variety of normal as well as pathological processes, we addressed the role of fatty acid synthase (FASN) in profibrotic TGF-β signaling as it has been shown to be critical for the progression of numerous human tumors. We found that FASN is required for the fibroproliferative actions of TGF-β in both cell culture as well as a murine model of lung fibrosis. Thus, our findings suggest that a similar approach might provide an effective antifibrotic therapy for pulmonary fibrosis and/or other fibrotic disorders.

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