Associate Professor, Department of Pharmaceutical Sciences
Dr. Charles Loftin
Dr. Loftin received a Ph.D. in Toxicology in 1995 from the University of North Carolina at Chapel Hill and a B.S. in Pharmacy in 1989 from Auburn University. Before joining the University of Kentucky, Dr. Loftin was a Research Fellow with the National Institute of Environmental Health Sciences in Research Triangle Park, North Carolina.
Dr. Loftin's lab studies the functions of prostanoids, which are lipid mediators formed by most tissues and best known for producing inflammation. Prostanoids are synthesized by the cyclooxygenases that are better known as COX-1 and COX-2. The COX enzymes are targets of nonsteroidal anti-inflammatory drugs, such as aspirin and ibuprofen, and the COX-2-selective inhibitor celecoxib. By utilizing pharmacological inhibitors of the COX enzymes together with mice genetically deficient in either COX-1 or COX-2, Dr. Loftin's lab has identified a variety of different physiological and pathophysiological processes that are dependent on either COX-1 or COX-2. These include prenatal and postnatal vascular development, protection against pathogen-induced atherosclerosis, adipose tissue differentiation, vascular remodeling associated with aortic aneurysm initiation and progression, and vascular smooth muscle cell phenotypic modulation. The goal of this work is to identify targets down-stream of the COX isoforms that will lead to the development of medications with novel therapeutic benefit and which lack the adverse effects of currently available COX inhibitors.
Loftin Charles D. (2016). Microsomal Prostaglandin E Synthase-1 Expression by Aortic Smooth Muscle Cells Attenuates the Differentiated Phenotype.
Oestreich J H, Steinhubl S R, Ferraris Suellen Prins, Loftin Charles D, Akers W S. (2014). Effect of genetic variation in P2Y12 on TRAP-stimulated platelet response in healthy subjects.Journal of thrombosis and thrombolysis, 38(3), 372-9.
Oestreich J H, Steinhubl S R, Ferraris S P, Loftin Charles D, Akers W S. (2014). Effect of genetic variation in P2Y12 on TRAP-stimulated platelet response in healthy subjects.J Thromb Thrombolysis,
Trivedi D B, Loftin Charles D, Clark J, Myers P, DeGraff L M, Cheng J, Zeldin D C, Langenbach R. (2013). β-Arrestin-2 deficiency attenuates abdominal aortic aneurysm formation in mice.Circ Res, 112((9)), 1219-29.