How Glucocorticoid Drugs Protect The Heart
- Date:
- May 20, 2009
- Source:
- Journal of Clinical Investigation
- Summary:
- Synthetic glucocorticoids are used clinically in many situations, such as to treat asthma, and have been shown in animals and humans to help protect the heart from the damaging effects of heart attack. This has previously been attributed to their anti-inflammatory effects, however new research now indicates there is another mechanism by which glucocorticoids protect rodent hearts from the damaging effects of heart attack: they induce heart muscle cells to produce the protective molecule PGD2.
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Glucocorticoids are steroid hormones that have numerous functions; for example, they regulate the response to stress and suppress inflammation. Synthetic glucocorticoids are used clinically in many situations, most famously to treat asthma, allergies, and autoimmunity.
They have also been shown in animals and humans to help protect the heart from the damaging effects of heart attack, and this has been attributed to their anti-inflammatory effects. However, Motoaki Sano and colleagues, at Keio University School of Medicine, Japan, have now determined another mechanism by which glucocorticoids protect rodent hearts from the damaging effects of heart attack.
Specifically, glucocorticoids, acting via the glucocorticoid receptor (GR), induced mouse and rat heart muscle cells to produce PGD2, and this was responsible for the ability of glucocorticoids to reduce damage to mouse hearts in both an ex vivo and an in vivo model of heart attack.
The authors therefore suggest that GR-selective glucocorticoids might be more beneficial to humans following heart attack than glucocorticoids that activate both GR and the MR protein, activation of which occurs in response to stress and might have unwanted consequences.
Story Source:
Materials provided by Journal of Clinical Investigation. Note: Content may be edited for style and length.
Journal Reference:
- Glucocorticoid protects rodent hearts from ischemia/reperfusion injury by activating lipocalin-type prostaglandin D synthase%u2013derived PGD2 biosynthesis. Journal of Clinical Investigation, May 17, 2009
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