Calcitonin, a well-known thyroid hormone that helps regulate bone mass and collagen production, is also produced by cells in the heart, researchers in Canada, the U.S., the U.K. and Australia have found. Published in Nature, their breakthrough promises to aid in developing new treatments for people with atrial fibrillation (AF), a common heart-rhythm disorder.
“This discovery could provide important advances for patients with AF,” said senior co-author Stanley Nattel, a cardiologist at the Montreal Heart Institute and professor at Université de Montréal, who conducted the research with colleagues at Oxford University, the Baylor College of Medicine and the University of Melbourne.
“With a better understanding of calcitonin and its role in regulating fibrosis in the heart, we can now explore how to best restore the actions of this hormone, aiming to develop new treatments for AF patients,” said Nattel.
Levels of calcitonin in the body decrease with age, the main risk factor for developing AF, the most common heart-rhythm disorder and one associated with significant morbidity and mortality, particularly the risk of stroke.
Scarring (or fibrosis, in medical parlance) of the atria, the upper chambers of the heart, is caused by the accumulation of collagen, a protein found in skin and connective tissues. This fibrosis both predisposes people to AF and makes AF harder to treat.
In their study, Nattel and his colleagues found that the atrial muscle cells produce approximately 16 times more calcitonin than cells in the thyroid gland which, up until now, was thought to be by far the most important source of calcitonin in the body.
The researchers also found calcitonin receptors in specialized atrial cells, called fibroblasts, responsible for producing collagen and found that calcitonin acts to keep their collagen production in check. In AF patients, something goes wrong to impair the protective actions of calcitonin, increasing their risk.
Around 200,000 Canadians are affected by AF. To date, treatment has focused on restoring a normal heart rhythm, controlling the rate at which the heart beats and prescribing blood thinners to reduce the risk of stroke.
No treatment option is available to address the scarring of the atria seen in people with the condition. The new research could be key to identifying valuable new treatment options to address this.
Source: University of Montreal