title: Exploiting the Pleiotropic Antioxidant Effects of Established Drugs in Cardiovascular Disease.
abstract: Cardiovascular disease is a leading cause of death and reduced quality of life worldwide. Arterial vessels are a primary target for endothelial dysfunction and atherosclerosis, which is accompanied or even driven by increased oxidative stress. Recent research in this field identified different sources of reactive oxygen and nitrogen species contributing to the pathogenesis of endothelial dysfunction. According to lessons from the past, improvement of endothelial function and prevention of cardiovascular disease by systemic, unspecific, oral antioxidant therapy are obviously too simplistic an approach. Source- and cell organelle-specific antioxidants as well as activators of intrinsic antioxidant defense systems might be more promising. Since basic research demonstrated the contribution of different inflammatory cells to vascular oxidative stress and clinical trials identified chronic inflammatory disorders as risk factors for cardiovascular events, atherosclerosis and cardiovascular disease are closely associated with inflammation. Therefore, modulation of the inflammatory response is a new and promising approach in the therapy of cardiovascular disease. Classical anti-inflammatory therapeutic compounds, but also established drugs with pleiotropic immunomodulatory abilities, demonstrated protective effects in various models of cardiovascular disease. However, results from ongoing clinical trials are needed to further evaluate the value of immunomodulation for the treatment of cardiovascular disease.
authors.affiliation: Medical Clinic, University Medical Center of the Johannes Gutenberg-University, Mainz 55131, Germany. Sebastiansteven@gmx.de.|Center for Thrombosis and Hemostasis, University Medical Center of the Johannes Gutenberg-University, Mainz 55131, Germany. Sebastiansteven@gmx.de.
authors.forename: Sebastian
authors.initials: S
authors.lastname: Steven
authors.affiliation: Medical Clinic, University Medical Center of the Johannes Gutenberg-University, Mainz 55131, Germany. tmuenzel@uni-mainz.de.
authors.forename: Thomas
authors.initials: T
authors.lastname: Münzel
authors.affiliation: Medical Clinic, University Medical Center of the Johannes Gutenberg-University, Mainz 55131, Germany. daiber@uni-mainz.de.
authors.forename: Andreas
authors.initials: A
authors.lastname: Daiber
mesh_terms: D000818:Animals; D000975:Antioxidants / Q000627:therapeutic use*; D002318:Cardiovascular Diseases / Q000188:drug therapy* / Q000276:immunology / Q000378:metabolism / Q000473:pathology; D004730:Endothelium, Vascular / Q000187:drug effects / Q000276:immunology / Q000378:metabolism / Q000473:pathology; D004763:Glucagon-Like Peptides / Q000031:analogs & derivatives / Q000627:therapeutic use; D006801:Humans; D007155:Immunologic Factors / Q000627:therapeutic use*; D007249:Inflammation / Q000188:drug therapy / Q000276:immunology / Q000378:metabolism / Q000473:pathology; D018384:Oxidative Stress / Q000187:drug effects
chemical_list: D000975:Antioxidants; D007155:Immunologic Factors; D004763:Glucagon-Like Peptides
keywords: cardiovascular disease; dipeptidyl peptidase-4 inhibitors; endothelial dysfunction; glucagon-like peptide analogs; inflammation; oxidative stress