New Discovery Offers Hope in Preventing Heart Failure Post-Heart Attack

Researchers at UC San Diego have identified a new mechanism of cardiac inflammation that might prevent heart attacks from progressing to heart failure. The findings, from Dr. Kevin King's lab, suggest that targeting inflammation in the heart's borderzone could offer new therapeutic opportunities.

UC San Diego researchers have unveiled a promising new mechanism in cardiac inflammation that could prevent heart attacks from progressing to heart failure. According to their study published in the Aug. 28, 2024 issue of Nature, targeting inflammation in the heart's borderzone may offer new therapeutic opportunities.

The research team, led by Dr. Kevin King, pinpointed a surprising driver of inflammation: heart muscle cells or cardiomyocytes. Typically, professional immune cells are credited with post-heart attack inflammation. However, the team discovered that cardiomyocytes in the borderzone, a challenging yet crucial area, activate proinflammatory type I interferon (IFN) responses under mechanical stress.

This discovery opens the door to novel treatments aimed at limiting mechanical stress, inhibiting DNA sensing, and preventing type I IFN signaling in the borderzone. Such therapies may help patients avoid the debilitating progression from heart attack to heart failure, emphasizing the clinical significance of these findings from Dr. King's lab.

(With inputs from agencies.)