Scientists searching for a therapy to stop idiopathic pulmonary fibrosis found a new molecular target that slows or stops the illness in preclinical laboratory tests.

A research team at Cincinnati Children’s Hospital Medical Center reports its data in the journal Cell Reports. It found that a gene called FOXF1 inhibits the IPF disease process, which includes extensive scarring in lung connective tissues, hyperproduction of harmful cells called myofibroblasts and excessive lung inflammation.

Their data show human lungs from IPF patients and mouse models of IPF lack FOXF1 in myofibroblasts. But cells lacking FOXF1 also exhibit overexpression of a related gene called FOXM1, which drives lung scarring and inflammation.

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