Cookies on this website

We use cookies to ensure that we give you the best experience on our website. If you click 'Accept all cookies' we'll assume that you are happy to receive all cookies and you won't see this message again. If you click 'Reject all non-essential cookies' only necessary cookies providing core functionality such as security, network management, and accessibility will be enabled. Click 'Find out more' for information on how to change your cookie settings.

A hormone which helps regulate bone mass is also produced by the heart and could help treat people with a dangerous heart rhythm disorder, according to a new study published in the journal Nature.

A hormone which helps regulate bone mass is also produced by the heart and could help treat people with a dangerous heart rhythm disorder, according to a new study published in the journal Nature.

Until now, the hormone calcitonin was only thought to be produced by the thyroid gland, with no known effects on the heart. The new study revealed that cells in the upper chambers of the heart (the atria) produce approximately 16 times more calcitonin than cells in the thyroid.

The researchers at the Radcliffe Department of Medicine, led by Associate Professor Svetlana Reilly, also found that the hormone plays a vital role in reducing atrial scarring. Such scarring makes it harder for electrical impulses to travel smoothly through the atria and can cause them to beat in a chaotic manner, known as atrial fibrillation (AF).

For a long time we’ve known the heart only produces a small number of hormones, and we can now add a new one to the list.
- Associate Professor Svetlana Reilly

The research team studied muscle cells from atrial biopsies taken from people undergoing heart surgery and found that they released calcitonin. Interestingly, cells from biopsies of patients with severe AF produced six times less calcitonin.


Looking further, they saw that the calcitonin receptor was present in atrial cells responsible for producing collagen, a major component of scar tissue. When the team treated these cells - called fibroblasts - with calcitonin the cells produced 46 per cent less collagen.


Further experiments showed that mice which were unable to produce calcitonin in their hearts developed 2.5 times more atrial scar tissue, compared to mice with normal levels of calcitonin. They also developed AF at a younger age and had approximately 16 times longer episodes of AF. Strikingly, atrial scarring and AF were completely prevented in mice whose hearts produced greater amounts of calcitonin.

Atrial fibrillation

Around 1.4 million people in the UK have been diagnosed with atrial fibrillation, which can significantly increase a person’s risk of stroke by promoting the formation of blood clots in the heart that may then travel to the brain and block blood vessels there.


Researchers now hope that this new heart hormone and its receptor may hold the key to treating this potentially devastating condition.


Professor Svetlana Reilly, BHF Intermediate Fellow at the Radcliffe Department of Medicine, said: “Discovering that calcitonin is released by the heart should open new doors for developing heart treatments.

“It looks as though calcitonin and its receptor might have been an important missing piece to the atrial fibrillation puzzle.

“We now need to explore how we can best restore the actions of this hormone to treat people with this type of AF, and to understand when the best time to treat someone would be."

Professor Metin Avkiran, Associate Medical Director at the British Heart Foundation, said: “Many of the treatments available for AF focus on restoring a normal atrial rhythm, controlling the rate at which the heart beats or thinning the blood to reduce the risk of stroke - but they do not tackle the atrial scarring seen in people with severe AF.

“These discoveries could be game-changing for the management of AF. Developing a new treatment to prevent or reverse atrial scarring could provide a lifeline to many people at risk of or living with AF.”


This work was an international collaboration with the University of Montreal, Baylor College of Medicine in USA and University of Melbourne.

Read the full paper