First-responder cells launching the repair after a heart attack are so frantic about fixing the damage that they promote more inflammation than necessary, new research in mice suggests.
First-responder cells launching the repair after a heart attack are so frantic about fixing the damage that they promote more inflammation than necessary, new research in mice suggests.
Based on those findings, scientists are pursuing interventions that would bring more balance to the healing process after a heart attack.
In a series of studies, the researchers have identified the cellular events that lead to a call for reinforcements – an extra wave of the first responders – to the site of repair. This process leads to the release of proinflammatory proteins at a point when they aren’t needed, creating conditions that may threaten optimum healing of the heart.
The first-responder cells in question are neutrophils, the most abundant of all white blood cells whose job is to heal wounds and clear away infection. Researchers are exploring potential drugs or genetic techniques that could block the call for neutrophil backups or limit the release of proteins that drive up inflammation.
Read more at: Ohio State University
