Endothelial Cells: From Dysfunction Mechanism to Pharmacological Effect in Cardiovascular Disease

Endothelial cells (ECs) are the innermost layer of blood vessels that play important roles in homeostasis and vascular function. However, recent evidence suggests that the onset of inflammation and the production of reactive oxygen species impair the function of ECs and are a main factor in the development of cardiovascular disease (CVD). In this study, we investigated the effects of inflammatory markers, oxidative stress, and treatment on ECs in CVD patients. This review article is based on the material obtained from PubMed up to 2018. The key search terms used were "Cardiovascular Disease," "Endothelial Cell Dysfunction," "Inflammation," "Treatment," and "Oxidative Stress." The generation of reactive oxygen species (ROS) as well as reduced nitric oxide (NO) production by ECs impairs the function of blood vessels. Therefore, treatment of CVD patients leads to the expression of transcription factors activating anti-oxidant mechanisms and NO production. In contrast, NO production by inflammatory agents can cause ECs repair due to differentiation of endothelial progenitor cells (EPCs). Therefore, identifying the molecular pathways leading to the differentiation of EPCs through mediation of factors induced by inflammatory factors can be effective in regenerative medicine for ECs repair.