Researchers at the University of Alabama at Birmingham (UAB) have identified a new molecular target that could prove useful in the potential treatment of the deadly, aging-related lung disease idiopathic pulmonary fibrosis (IPF). The study, which was published online on March 10. 2021 in the Journal of Experimental Medicine (JEM)( https://rupress.org/jem/article-lookup/doi/10.1084/jem.20202033?PR), suggests that targeting a protein called MDM4 could prevent respiratory failure by initiating a genetic program that removes scar tissue from the lungs. The open-access article is titled “Targeting Mechanosensitive MDM4 Promotes Lung Fibrosis Resolution in Aged Mice.” IPF is characterized by the accumulation of scar tissue that stiffens the lungs and makes it difficult for patients to breathe and get sufficient oxygen into their blood. Though the causes of IPF remain unclear, age is a significant risk factor: the disease is estimated to affect 1 in 200 US adults over the age of 70. The scars are thought to arise from a runaway wound healing process in which lung cells deposit excessive amounts of collagen into their surroundings, stiffening the lung tissue and activating highly contractile cells called myofibroblasts. These myofibroblasts produce still more collagen fibers and stiffen the tissue even further. "Lung fibrosis resolution is thought to involve degradation of excessive collagen, removal of myofibroblasts, and regeneration of normal lung tissue by stem cells," says Yong Zhou, MD, PhD, an Associate Professor in the Department of Medicine, UAB. "However, the mechanisms underlying the reversal of lung fibrosis remain poorly understood."
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