Ischemic heart disease is the most common cause of death in the world. It begins with a "heart attack", also known as a myocardial infarction (MI), which causes part of the heart to die due to inadequate coronary blood flow. This leads to vigorous inflammation, heart wall remodeling, and heart failure.
Anti-inflammatory drugs have been surprisingly ineffective at preventing heart failure. As a consequence, they are not a routine part of post-MI care. However, it is possible that the most potent molecular and cellular inflammation targets have yet to be discovered.
In the Aug. 28, 2024 issue of Nature , researchers from University of California San Diego in the laboratory of Dr. Kevin King, associate professor of bioengineering and medicine, and a cardiologist at the Sulpizio Cardiovascular Center, report the discovery of a novel mechanism of cardiac inflammation that may expand therapeutic opportunities to prevent heart attacks from becoming heart failure.
Inflammation after MI is classically credited to professional immune cells like neutrophils and macrophages that infiltrate the infarcted heart and respond to molecules in the debris of dying cells. So the team was surprised when they discovered that the proinflammatory "type I interferon (IFN) response" was activated, not in the infarct where immune cells were concentrated, but instead in the borderzone, surrounding the infarct. The borderzone has been a fascinating yet understudied area of the infarcted heart.
It is where.