Under-activity of a gene called FOXF1 underlies lung damage in idiopathic pulmonary fibrosis
A new approach to treat an incurable disease has been made possible by the identification of a biological switch which 'turns off' cells that scar the lungs. The build-up of scars in idiopathic pulmonary fibrosis (IPF) makes the lungs stiffer and less elastic, making it harder to breathe. Treatments aim to slow this build-up, but there's no cure. The new research shows that patients and mice with the disease have unusually high levels of cells called myofibroblasts, which repair wounds by laying down layers of strong collagen. Normally, when a wound is sufficiently healed, the cells are switched off by the gene FOXF1. This study shows that IPF patients have low levels of FOXF1, so the cells remain active and drive an excessive build-up of collagen, as shown here (red) in mouse lung tissue (green). Treatments to ramp up FOXF1 activity could keep cells in check, making lungs healthier for longer.
Written by Deborah Oakley
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