Our Research

Our overall mission is to identify cellular and molecular mechanisms underlying failed inflammation-resolution programs in atherosclerosis and aging. 

Persistent, non-resolving inflammation is the underpinning of several prevalent human diseases. Therefore, understanding cellular and molecular mechanisms that promote the resolution of inflammation (or inflammation-resolution) is an unmet clinical need.

 The resolution response is in part mediated by specialized pro-resolving mediators, that include resolvins. We recently found that key resolvins protect against atherosclerosis and limit several features of aging.

Macrophages are key players in atherosclerosis and aging . They take cues from their local environment and so understanding how to reprogram macrophages to resolve and repair as opposed to promote inflammation is a major focus of the lab.