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FOXM1 Is a Critical Driver of Lung Fibroblast Activation and Fibrogenesis

FOXM1 Is a Critical Driver of Lung Fibroblast Activation and Fibrogenesis

Loka R Penke, Jennifer M Speth, Vijaya L Dommeti, Eric S White, Ingrid L Bergin, Marc Peters-Golden

J Clin Invest. 2018 Jun 1;128(6):2389-2405.

PMID: 29733296

Abstract:

While the transcription factor forkhead box M1 (FOXM1) is well known as a proto-oncogene, its potential role in lung fibroblast activation has never been explored. Here, we show that FOXM1 is more highly expressed in fibrotic than in normal lung fibroblasts in humans and mice. FOXM1 was required not only for cell proliferation in response to mitogens, but also for myofibroblast differentiation and apoptosis resistance elicited by TGF-β. The lipid mediator PGE2, acting via cAMP signaling, was identified as an endogenous negative regulator of FOXM1. Finally, genetic deletion of FOXM1 in fibroblasts or administration of the FOXM1 inhibitor Siomycin A in a therapeutic protocol attenuated bleomycin-induced pulmonary fibrosis. Our results identify FOXM1 as a driver of lung fibroblast activation and underscore the therapeutic potential of targeting FOXM1 for pulmonary fibrosis.

Chemicals Related in the Paper:

Catalog Number	Product Name	Structure	CAS Number	Price
AP12656096	Siomycin A		12656-09-6	Price

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