Invited Review ArticleGreen Tea and Heart HealthNaito, Yuji MD, PhD; Yoshikawa, Toshikazu MD, PhDAuthor Information From the Department of Molecular Gastroenterology and Hepatology, Kyoto Prefectural University of Medicine, Kyoto, Japan. Received for publication May 10, 2009; accepted June 22, 2009. The authors report no conflicts of interest. Reprints: Yuji Naito, MD, PhD, Department of Molecular Gastroenterology and Hepatology, Kyoto Prefectural University of Medicine, Kamigyo-ku, Kyoto 602-8566, Japan (e-mail: firstname.lastname@example.org). Journal of Cardiovascular Pharmacology: November 2009 - Volume 54 - Issue 5 - p 385-390 doi: 10.1097/FJC.0b013e3181b6e7a1 Buy Metrics Abstract The adherence of monocytes to vascular endothelial cells is an important early event in atherogenesis. Monocyte adherence to endothelial cells is induced by oxidized low-density lipoprotein (LDL) and mediated by multiple cell-adhesion molecules, including vascular cell-adhesion molecule 1 and intercellular cell-adhesion molecule 1. Enhanced endothelial expression of these molecules by oxidized LDL has been shown to be a critical step in foam cell formation and the development of atherosclerosis. Recent studies have demonstrated that tea catechin, especially (−)-epigallocatechin-3-gallate, inhibits the expression of these molecules by endothelial cells in response to stimulation with oxidized LDL or inflammatory cytokines and the expression of CD11b by monocytic leukocytes. An in vivo study using apolipoprotein E-deficient mice has demonstrated that tea catechin extracts prevent the development of atherosclerosis and that (−)-epigallocatechin-3-gallate effectively reduces the progression of accelerated atherosclerotic plaque formation induced by cuff injury. These data suggest that tea catechin may provide a unique approach to reduce atherosclerosis, although further studies will be necessary to clarify the precise mechanism of these effects, especially the role of metabolites of catechin and the target sites of these compounds. © 2009 Lippincott Williams & Wilkins, Inc.