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Zinc Found to Play an Important Role in Lung Fibrosis

Cedars-Sinai Research Shows Targeting a Newly Identified Molecular Pathway With a Common Mineral Could Help Reverse Lung Damage in Idiopathic Pulmonary Fibrosis Patients

Investigators from the Women’s Guild Lung Institute at Cedars-Sinai have discovered that zinc, a common mineral, may reverse lung damage and improve survival for patients with a deadly age-related condition known as idiopathic pulmonary fibrosis (IPF).

Their findings, published in The Journal of Clinical Investigation, have the potential to change the landscape of treatment for patients which most often affects those over age 50.

“This study has the potential to be a game changer,” said Paul Noble, MD, chair of the Department of Medicine, director of the Women’s Guild Lung Institute and co-senior author of the study. “We identified a root cause of IPF-related lung damage and a potential therapeutic target that might restore the lungs’ ability to heal themselves.”

Idiopathic pulmonary fibrosis, or IPF, affects 100,000 people in the U.S. and has no known cause. The condition, which leads to scarring of the lungs, called fibrosis, and progressive breathing difficulty, has no cure, and most patients die or require a lung transplant within three to five years of diagnosis. The incidence of IPF rises dramatically with age and affects men more often than women.

Through this research, Cedars-Sinai investigators found that stem cells lining the air sacs in the lungs of patients with IPF lose their ability to process zinc, which is known to have a role in the growth of cells and healing damaged tissue.

Lack of zinc impairs the ability of the cells—called type 2 alveolar epithelial cells (AEC2s)—to regenerate. Restoring this ability via the molecular pathway the investigators traced in their experiments could lead to therapies that reverse IPF-related lung damage. The research team also generated a model of IPF in laboratory mice that can be used to develop new therapies.  Read More

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