Hearts Under Pressure: Disease at the Tipping Point

Heart disease starts quietly, as immune cells sneak into blood vessel walls and turn into fat-loaded “foam cells.” But how do they actually take up that fat? In my work, I use live imaging in mice to literally watch these cells in action. We found that instead of relying only on specific receptors, some immune cells “drink” their surroundings—a process called macropinocytosis—pulling in fluid, fat, and other molecules all at once. By tracking this behavior in real time and pairing it with molecular profiling, we can identify a unique group of highly active, fat-hungry cells inside plaques. Understanding this hidden pathway could open the door to new ways to detect and treat atherosclerosis earlier—before it leads to heart attacks or strokes.

Atrial fibrillation affects over 37 million people and can lead to stroke or death. Current treatments target electrical signals but miss a key driver: fibrosis, driven by inflammation that doesn’t stop. Inflammation is meant to heal, but beyond a critical threshold, it turns destructive. I study a protein that controls this switch, and using clinical and mouse models, I found that only its activated form predicts cardiac disease. When activated at the right time, it promotes recovery; when it fails, it leads to damage. This hidden switch could transform how we detect and treat heart disease.