Myocardial infarction (MI) or heart attack is the major cause of death in men and women in the United States. Because it interrupts the heart’s oxygen supply, MI causes irreversible tissue damage that can lead to heart failure.
A protein called Gremlin 2 (Grem2), which is required for early cardiac development, also is strongly induced in the heart after experimental MI. However, little is known about the function of Grem2 after cardiac injury.
Now, in a paper published recently in the journal Circulation Research, Antonis Hatzopoulos, Ph.D., and colleagues show that Grem2 provides a molecular barrier that controls the magnitude and extent of inflammation after MI.
They show that Grem2 suppresses the signaling of bone morphogenetic protein (BMP). BMP signaling plays an important role in heart development but its activation following ischemic injury regulates the inflammatory response.
Their findings suggest a new strategy to limit the adverse effects of excessive inflammation following MI.
This research was supported by grants from the National Institutes of Health (HL083958, HL100398, GM114640) and by institutional support from Vanderbilt University Medical Center.
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