Invited Review ArticleSmall GTPase and Regulation of Inflammation Response in AtherogenesisLu, Yuyan MD; Peng, Wenhui MD, PhD; Xu, Yawei MD, PhDAuthor Information Department of Cardiology, Shanghai Tenth People's Hospital, Tongji University School of Medicine, Shanghai, China. Reprints: Yawei Xu, MD, PhD, Department of Cardiology, Shanghai Tenth People's Hospital, Tongji University School of Medicine, 301 Middle Yanchang Road, Shanghai 200072, China (e-mail: firstname.lastname@example.org). Supported by the National Natural Science Foundation of China (No. 81270256). The authors report no conflicts of interest. Received April 13, 2013 Accepted June 18, 2013 Journal of Cardiovascular Pharmacology: October 2013 - Volume 62 - Issue 4 - p 331-340 doi: 10.1097/FJC.0b013e3182a12eb3 Buy Metrics Abstract Abstract: Small GTPases are key signal transducers from extracellular stimuli to the nucleus that regulate a variety of cellular responses, including changes in gene expression and cell adhesion and migration. Accumulating data have demonstrated that abnormal activation of these small GTPases plays a critical role in the atherosclerosis characterized by vascular abnormalities, especially endothelial dysfunction and inflammation. Here, we discuss the linkage between small GTPases, inflammation, and atherogenesis. First, small GTPases affect gene expression of inflammatory cytokines through proinflammatory signaling pathways, such as nuclear factor-κB, vascular cell adhesion molecule-1, intercellular adhesion molecule-1, interlukin-8, and monocyte chemoattractant protein-1. Then, these molecules regulate the vascular inflammation through cell adhesion and migration. In turn, small GTPases are also regulated by extracellular stimuli, such as L-selectin, thrombin, oxidized phospholipids, and interleukins. Thus, these inflammatory cytokines generate a vicious cycle for small GTPases and inflammatory responses in the atherogenesis. © 2013 by Lippincott Williams & Wilkins.