Researchers from the United States have found that two proteins that bind to stress hormones work together to maintain the health of the mouse heart. These proteins, known as the glucocorticoid receptor (GR) and the mineralocorticoid receptor (MR), act synergistically to help support heart health. When the signal between the two receptors is out of balance, the mouse will develop heart disease.
The researchers examined the specific and coordinated roles that these receptors played in mediating the direct effects of stress on the heart, they generated mice with cardiomyocyte-specific deletion of GR (cardioGRKO), MR (cardioMRKO), or both GR and MR (cardioGRMRdKO).
The cardioGRKO mice spontaneously developed cardiac hypertrophy and left ventricular systolic dysfunction and died prematurely from heart failure. In contrast, the cardioMRKO mice exhibited normal heart morphology and function. Despite the presence of myocardial stress, the cardioGRMRdKO mice were resistant to the cardiac remodeling, left ventricular dysfunction, and early death observed in the cardioGRKO mice.
Gene expression analysis revealed the loss of gene changes associated with impaired Ca2+ handling, increased oxidative stress, and enhanced cell death and the presence of gene changes that limited the hypertrophic response and promoted cardiomyocyte survival in the double knockout hearts. Reexpression of MR in cardioGRMRdKO hearts reversed many of the cardioprotective gene changes and resulted in cardiac failure.
These findings reveal a critical role for balanced cardiomyocyte GR and MR stress signaling in cardiovascular health.
“In the past, when researchers designed synthetic hormones for this task, the molecules they make work only on one receptor.” the researcher said, "We suggest that since GR and MR work together, a better approach is to make drugs that act on both receptors simultaneously. It can help heart patients to prevent subsequent heart disease."
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