Our overall mission is to identify cellular and molecular mechanisms underlying failed endogenous resolution programs in atherosclerosis and aging. To accomplish this goal, Dr. Fredman has established an NIH-funded research laboratory, and has established collaborative efforts with experts around the world.
Persistent, non-resolving inflammation is the underpinning of several prevalent diseases. The Fredman lab is exploring cellular and molecular mechanisms underlying defective inflammation resolution in atherosclerosis and aging.
The resolution response is in part mediated by specialized pro-resolving mediators (SPMs), which are endogenous lipid mediators actively generated during inflammation. SPM families include lipoxins, resolvins, protectins, and maresins and are biosynthesized from lipoxygenase- and cyclooxygenase-initiated mechanisms*. SPMs each possess distinct structures that bind and activate select cell surface receptors*. Dr. Fredman's lab is investigating the endogenous role of SPMs in atherosclerosis and aging.
*SPMs discovered by Dr. Charles Serhan (Brigham and Women's Hospital/Harvard Medical School)