Not following a regular sleep schedule can result in deadly lung diseases, a new study has found.
The study, published in the journal Nature Communications, noted that irregular sleeping patterns can adversely affect the body’s natural biological clock (also known as the circadian clock), which can lead to lung scarring or pulmonary fibrosis, a potentially deadly disease in which connective tissue builds up in the lungs, hardening them and causing breathing difficulties.
It comes down to a protein associated with the circadian clock called REV-ERBα, a circadian rhythm protein that regulates collagen production in the body. Lack of REV-ERBα can help boost collagen production which, in turn, can cause the hardening of lung tissues and eventually fibrosis.
The team behind the study, led by Irfan Rahman, Ph.D., Dean’s Professor of Environmental Medicine at the University of Rochester Medical Center, found low levels of REV-ERBα and increased levels of collagen and lysyl oxidase in lung samples of pulmonary fibrosis patients, according to Hindustan Times.
In a mouse model study, researchers found that the REV-ERBα fluctuates throughout the day, peaking in the noon time and dropping during the night. When dealt an injury at night, mice models showed larger increases in lysyl oxidase and collagen proteins, wider lung damage and lower survival rates compared to mice harmed during the daytime.
Rahman said night-shift employees are more at risk of the condition. “Night-shift work usually occurs around midnight, when the expression of REV-ERBα is at its lowest,” he explained. “Our findings suggest that REV-ERBα activation at night provides less protection against lung fibrosis.”
Qixin Wang, Ph.D., a postdoctoral fellow working in Rahman’s lab, said in the study that the market lacks enough fibrosis medications, and with the new study, scientists are aiming to develop new drugs to better treat the lung condition.
“Currently, there are only two drugs approved by the FDA to treat fibrosis, and they only delay the process, they don’t cure the disease,” Wang said. “REV-ERBα-activating drugs could serve as potential therapeutics to help prevent fibrosis and stop the disease process.”
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