Hormone signalling mechanisms in heart failure require a functional circadian rhythm.

Lead researcher

Dr Morag Young

Main finding

This study showed that two important cell signalling processes that lead to heart disease influence each other to modify disease mechanisms in cardiac muscle cells and inflammatory cells.

We have previously shown that inappropriate activation of the steroid hormone receptor the MR (mineralocorticoid receptor) causes cardiac tissue inflammation and fibrosis.


Centre for Endocrinology and Metabolism

Research group

Cardiovascular Endocrinology


Elizabeth K. Fletcher
James Morgan1,2,
Professor David Kennaway
Laura A. Bienvenu
Dr Amanda J. Rickard
Prof Lea M.D Delbridge
Prof Peter J. Fuller
A Prof Colin D. Clyne
Dr Morag J. Young

Journal and article title

Most surprising

We were excited to find that the typical heart disease processes and features caused by excess MR signalling in our mouse model were blunted in mice that contained no circadian rhythm.

We found several patterns of response that give us new insights into how important the combination of circadian signalling and MR signalling is.

First, the mice lacking a circadian rhythm had increased heart size, this was expected. The addition of MR activation made the hearts larger. This is normally a bad outcome.

However the inflammatory processes in the hearts were significantly low.

Less inflammatory cells were recruited to the heart.

This resulted in much lower fibrosis or connective tissue in the heart, which would result in a heart that functions better.

Future implications

This study reveals a new signalling pathways that interacts with or influences the MR and thus MR-mediated heart disease.
It also reveals a very interesting biology, where the MR can modify circadian signalling in cardiac tissue. Until now, it was thought that adrenal steroids acting via the GR could regulate tissue circadian clocks.

Disease/health impact

heart failure