Understanding the role of hibernating cells in atherosclerosis

Do IL-1R2 and inflammatory caspases regulate IL-1 in senescence and atherosclerosis?

Atherosclerosis is the build-up of fatty material inside arteries, and it causes most heart attacks and strokes. An important process in atherosclerosis is inflammation within the blood vessel wall. This is thought to be caused in part by damaged cells that escape death and ‘hibernate’. These cells stop dividing and behave differently to normal cells, allowing them to contribute to inflammation. These hibernating cells use a molecule called Interleukin-1 (IL-1) to drive inflammation and Dr Clarke thinks this process could be blocked by a protein called IL-1 receptor 2 (IL-R2). His fellowship will investigate this theory. He hopes to determine whether white blood cells called neutrophils control inflammation by producing IL-1R2 that circulates in the blood and blocks the function of IL-1. He also will investigate whether two molecules involved in inflammation and in cell death (called caspases) control the release of inflammatory molecules from hibernating cells. Ultimately, he hopes to determine whether these hibernating damaged cells cause harm to the blood vessels because they’ve changed their function, cause inflammation, or both. An in-depth understanding of their role in blood vessel inflammation will help guide both the development and testing of new drugs to treat heart disease.