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The study, published in the journal PNAS, also shows that tuning the body clock reduces fibrosis or lung scarring in cell studies, revealing a potential target for this killer disease.
Pulmonary fibrosis occurs when the lung tissue becomes damaged and scarred, making it more difficult for the organ to work properly.
The researchers, including those from the universities of Manchester, and Oxford in the UK noted that our internal body clock regulates nearly every cell in the human body.
The clock drives 24-hour cycles in many processes such as sleeping, hormone secretion, and metabolism.
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However, the team discovered that in people with lung fibrosis, these clock oscillations extend out to the small air spaces, called alveoli.
“Pulmonary fibrosis is a devastating condition which is incurable at present,” said John Blaikley from The University of Manchester, who led the project.
“Therefore, the discovery that the body clock is potentially a key player potentially opens new ways to treat or prevent the condition,” Blaikley said in a statement.
Studies in mice revealed that by altering the clock mechanism it was possible to disrupt the fibrotic process making the animals more likely to develop pulmonary fibrosis.
The researchers then showed, that pulmonary fibrosis is associated with short and long sleep duration using human data from the UK Biobank, a research resource containing health and genetic information for half a million people.
The link between sleep duration and lung fibrosis is similar in strength to other known risk factors for this disease, the researchers said.
People who report that they regularly sleep for four hours or less in a day doubled their chance of having pulmonary fibrosis, while those sleeping 11 hours or longer in a day tripled their chance of having the disease, compared to those sleeping seven hours per day.
Smaller, but still elevated, risks were also seen in people who like to stay up late at night, or those who do shift work, the researchers said.
They explain their findings by discovering that a core clock protein (REVERBa) which alters the production of a key protein in lung fibrosis (collagen).
This is an exciting finding because chemical compounds can alter the function of REVERBa, the researchers said.
They were able to show that one of these REVERBa compounds can reduce collagen in lung slices taken from people with this disease.
The researchers said more work is needed to study the association between pulmonary fibrosis and sleep duration to establish both causation and reproducibility.
“If these results are confirmed, then sleeping for the optimal time may reduce the impact of this devastating disease,” said Blaikley.