Zinc supplements could reverse lung damage, new study finds

Researchers from the Women’s Guild Lung Institute at Cedars-Sinai have discovered that zinc may reverse lung damage and improve survival for patients with idiopathic pulmonary fibrosis (IPF), according to their findings published in The Journal of Clinical Investigation.

This breakthrough study has the potential to change the landscape of treatment for patients with IPF, a deadly age-related condition that affects 100,000 people in the U.S. and has no known cause. Most patients die or require a lung transplant within three to five years of diagnosis.

“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 is a condition that leads to scarring of the lungs, called fibrosis, and progressive breathing difficulty. 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.

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In experiments with organoids—miniaturized, simplified versions of organs grown in a dish from patients’ tissues—they also observed that cells lacking the ZIP8 protein were unable to regenerate and form colonies as healthy cells should. ZIP8 is a protein that draws zinc into the cell.

“The organoids with AEC2 cells that had the ZIP8 transporter were able to draw zinc into the cells, and then were able to regenerate and form more colonies,” said Carol Liang, MD, MBA, associate professor of Medicine and first author of the study. “The cells without ZIP8 didn’t have a way to draw zinc in, so they formed fewer colonies. This is how we determined that it is ZIP8 that allows the cells to use zinc.”

The investigators also used medication and deletion of the ZIP8 gene in mouse AEC2s to mimic IPF in laboratory mice. When they fed these mice a diet that included zinc supplements, their fibrosis improved.

“There have been few detailed studies of how zinc works in the lungs,” said Dianhua Jiang, MD, PhD, professor of Medicine at Cedars-Sinai and co-senior author of the study. “Ours is the first to identify the detailed function of zinc in lung biology, specifically in IPF.

It was particularly exciting to discover that zinc regulates the production of two other key molecules that promote tissue regeneration, nicotinamide adenine dinucleotide (NAD+) and Sirtuin1. These molecules have been implicated in tissue regeneration and aging.”

Additional research is needed to help determine why the loss of ZIP8 occurs in the lung cells, and whether zinc supplements, alone or in combination with NAD+ and Sirtuin1 activators to help activate lung repair response, will reverse lung damage in human patients with this condition, Liang said, adding that answers to these questions could help thousands of patients.

The potential breakthrough in IPF treatment comes at a time when the medical community has been struggling to find a cure for the disease. Despite the best efforts of healthcare providers, IPF remains a major public health concern, affecting more people each year as the population ages.

The study’s findings offer hope for patients and their families who have been impacted by this devastating condition. While there is still much research to be done to understand the mechanisms behind the loss of ZIP8 and how zinc supplements can help reverse lung damage, the discovery of this molecular pathway is a significant step forward in the fight against IPF.

“This study has the potential to provide much-needed relief for patients suffering from IPF,” said Liang. “We hope to continue our research and ultimately develop a safe and effective treatment for this disease.”

The Women’s Guild Lung Institute at Cedars-Sinai has been at the forefront of IPF research for many years, and the latest findings build on previous work by the institute’s researchers. In 2019, a team of scientists led by Noble published a study in Nature Communications that identified a molecular pathway involved in lung regeneration and repair.

The study revealed that a protein called fibroblast growth factor 10 (FGF10) plays a critical role in promoting the growth and regeneration of lung tissue. The researchers found that by activating the FGF10 pathway in mice with damaged lungs, they were able to significantly improve lung function and reduce scarring.

The discovery of the ZIP8/NAD+/Sirtuin1 pathway represents another major breakthrough in the field of IPF research, and could pave the way for new treatments for the disease. While the study’s findings are still in the early stages, they offer a promising glimpse of what the future may hold for IPF patients.

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While providers now use stages I through IV for small cell lung cancer, you might also hear it described as limited or extensive stage. This is based on whether the area can be treated with a single radiation field.

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While there are many factors that can increase your risk of lung cancer, smoking any kind of tobacco products, including cigarettes, cigars or pipes is the biggest single risk factor. Experts estimate that 80% of lung cancer deaths are smoking-related.

Other risk factors include:

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