Monocyte and macrophage dysfunction has emerged as a fundamental process common to many chronic inflammation diseases and most complications associated with metabolic disorders, and thus has become a major focus for the design of new pharmacological and therapeutic interventions. We employ a wide array of biochemical, cell biological, imaging, and translational approaches to explore novel aspects of macrophage biology in the context of human vascular diseases and diabetic complications. Our approach is to build on fundamental discoveries at the molecular and cellular level and to translate these into animal models and ultimately, into patient settings.
Kim, H.S., Ullevig, L.S., Zamora, D. Lee, C.F. and Asmis, R. Redox Regulation of MAPK Phosphatase 1 Controls Monocyte Migration and Macrophage Recruitment. Proc.Natl.Acad.Sci., 109, E2803-12 (2012)
Ullevig, S., Zhao, Q., Zamora, D. and Asmis, R. Ursolic acid protects diabetic mice against monocyte dysfunction and accelerated atherosclerosis. Atherosclerosis, 219, 409-16 (2011).
Ullevig, S., Zhao, Q., Lee, C.F., Kim, H.S., Zamora, D. and Asmis, R. NADPH Oxidase 4 Mediates Monocyte Priming and Accelerated Chemotaxis Induced by Metabolic Stress. Arterioscler. Thromb.Vasc.Biol., 32, 415-26 (2012).
Lee CF, Qiao M, Schröder K, Zhao Q, Asmis R. Nox4 is a novel inducible source of reactive oxygen species in monocytes and macrophages and mediates oxidized low density lipoprotein-induced macrophage death. Circ Res. 2010 May 14;106(9):1489-97.
Tavakoli S, Zamora D, Ullevig S, Asmis R. Bioenergetic profiles diverge during macrophage polarization: implications for the interpretation of 18F-FDG PET imaging of atherosclerosis. J Nucl Med. 2013 Sep;54(9):1661-7.