Eugene A. Podrez, MD, PhD, is a member of Assistant Staff at Cleveland Clinic, and an Assistant Professor in Cleveland Clinic's Lerner College of Medicine of Case Western Reserve University. From 2001 to 2004, Dr. Podrez acted as Project Scientist in the Department of Inflammation & Immunity at Cleveland Clinic's Lerner Research Institute. He served as Postdoctoral Fellow and Research Associate from 1999 to 2001.
Dr. Podrez received his MD degree in 1982 from Moscow Medical University, Russia, and his PhD in cardiology in 1989 from the National Cardiology Research Center, Moscow. As a postgraduate student, he received additional training in cell biology and biochemistry at the National Cardiology Research Center, Moscow, from 1982 to 1984. He served as Junior Research Scientist, Research Scientist and then Senior Research Scientist at that institution from 1984 to 1994.
Awards & Honors
The major focus of our lab is how inflammation and oxidative stress contribute to atherosclerosis and thrombosis via lipid peroxidation and formation of bioactive lipids. Specifically, we are interested in how these conditions induce platelet “hyper-reactivity” associated with dislipoproteinemia, which is a known contributor to arterial thrombosis and plays an important role in atherosclerotic lesion formation. We are testing the hypothesis that platelets are activated in vivo by a recently discovered family of novel oxidized phospholipids. We have found that platelet scavenger receptors type B serve as sensors of specific oxidized phospholipids in plasma and mediate increased platelet reactivity in conditions of oxidative stress. This recognition leads to platelet activation and prothrombogenic status observed in hyperlipidemia, and may also account for platelet interactions with monocytes and endothelial cells in the initial stages of atherosclerosis development. Our research suggests that scavenger receptors type B on platelets may be the target for new therapies to reduce the risk of life-threatening events.
Our lab is also working towards elucidating the mechanisms of impairment of cholesterol efflux in cells in atherosclerosis. We have found that products of lipid oxidation may not only promote uptake of modified lipoproteins by macrophages via scavenger receptors, but these products can also interfere with cellular cholesterol efflux machinery and induce intracellular cholesterol accumulation by compromising cholesterol efflux.
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