Review ArticleDysfunctional Endothelial Progenitor Cells in Cardiovascular Diseases Role of NADPH OxidasePeng, Jun PhD*,†; Liu, Bin†; Ma, Qi-Lin MD, PhD‡; Luo, Xiu-Ju PhD*Author Information *Department of Laboratory Medicine, Xiangya School of Medicine, Central South University, Changsha, China; †Department of Pharmacology, School of Pharmaceutical Sciences, Central South University, Changsha, China; and ‡Department of Cardiovascular Medicine, Xiangya Hospital, Central South University, Changsha, China. Reprints: Xiu-Ju Luo, PhD, Department of Laboratory Medicine, Xiangya School of Medicine, Central South University, No. 172 Tongzipo Rd, Changsha 410013, China (e-mail: firstname.lastname@example.org), or Qi-Lin Ma, MD, PhD (e-mail: email@example.com). Supported by the National Nature Science Foundation of China (No. 81373409, 91439104 to J.P. and No. 81370250 to Q.-L.M.), Hunan Provincial Natural Science Foundation of China (No. 13JJ2008 to J.P.), and Doctoral Fund of Ministry of Education of China (No. 20120162110056 to J.P.). The authors report no conflicts of interest. Received May 28, 2014 Accepted September 02, 2014 Journal of Cardiovascular Pharmacology: January 2015 - Volume 65 - Issue 1 - p 80-87 doi: 10.1097/FJC.0000000000000166 Buy Metrics Abstract Abstract: Endothelial progenitor cells (EPCs) play a critical role in maintenance of the endothelial integrity and vascular homeostasis, as well as in neovascularization. Dysfunctional EPCs are believed to contribute to the endothelial dysfunction and are closely related to the development of various cardiovascular diseases, such as hypertension, hyperlipidemia, and stroke. However, the underlying mechanisms of EPC dysfunction are complicated and remain largely elusive. Recent studies have demonstrated that reactive oxygen species (ROS) are key factors that involve in modulation of stem and progenitor cell function under various physiologic and pathologic conditions. It has been shown that NADPH oxidase (NOX)–derived ROS are the major sources of ROS in cardiovascular system. Accumulating evidence suggests that NOX-mediated oxidative stress can modulate EPC bioactivities, such as mobilization, migration, and neovascularization, and that inhibition of NOX has been shown to improve EPC functions. This review summarized recent progress in the studies on the correlation between NOX-mediated EPC dysfunction and cardiovascular diseases. © 2015 by Lippincott Williams & Wilkins.