Two groups of rats, one with chronic kidney disease (CKD) and one with normal renal function, were exposed to cigarette smoke five days a week for four weeks. The smoke groups were compared with two control groups—one with CKD and the other with normal kidney function—that were kept in a room with no smoke.
Several factors associated with heart disease increased in the smoke groups, including blood pressure, enlargement of the heart and development of scar tissue in the heart muscle. Animals exposed to smoke also had fibrosis and reduced function in the kidneys.
Researchers examined genetic material (microRNA) in the organ tissue. They found that expression of the anti-fibrotic microRNA was significantly decreased in the smoke groups as compared to the control groups. Anti-fibrosis microRNA are the presence of small RNA molecules that are associated with slowing or preventing fibrosis.
The rat model of fibrosis paves the way for a similar exploration of genetic expression in humans. “This is a significant and novel finding illustrating the effects of tobacco and nicotine on epigenetic regulation of fibrosis formation in cardiac and renal tissues,” the authors wrote.
The article, “Cigarette Smoking Causes Epigenetic Changes Associated With Cardiorenal Fibrosis,” is published in Physiological Genomics.
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