AI Article Synopsis
- Corticosteroids impact heart development, function, and response to stress through glucocorticoid (GR) and mineralocorticoid (MR) receptors.
- The levels of these steroids are mainly regulated by the HPA axis, but an enzyme, 11β-HSD1, can convert inactive metabolites back to active glucocorticoids, increasing their local concentration in tissues.
- Recent research has focused on the role of 11β-HSD1 in the heart, suggesting it influences heart growth and function, and proposing it as a potential target for therapies aimed at improving recovery after heart attacks and preventing heart failure.
Article Abstract
Corticosteroids influence the development and function of the heart and its response to injury and pressure overload via actions on glucocorticoid (GR) and mineralocorticoid (MR) receptors. Systemic corticosteroid concentration depends largely on the activity of the hypothalamic-pituitary-adrenal (HPA) axis, but glucocorticoid can also be regenerated from intrinsically inert metabolites by the enzyme 11β-hydroxysteroid dehydrogenase type 1 (11β-HSD1), selectively increasing glucocorticoid levels within cells and tissues. Extensive studies have revealed the roles for glucocorticoid regeneration by 11β-HSD1 in liver, adipose, brain and other tissues, but until recently, there has been little focus on the heart. This article reviews the evidence for glucocorticoid metabolism by 11β-HSD1 in the heart and for a role of 11β-HSD1 activity in determining the myocardial growth and physiological function. We also consider the potential of 11β-HSD1 as a therapeutic target to enhance repair after myocardial infarction and to prevent the development of cardiac remodelling and heart failure.
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|---|---|
| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5148800 | PMC |
| http://dx.doi.org/10.1530/JME-16-0128 | DOI Listing |
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