title: Redox Roles of Reactive Oxygen Species in Cardiovascular Diseases.
abstract: Cardiovascular disease (CVD), a major cause of mortality in the world, has been extensively studied over the past decade. However, the exact mechanism underlying its pathogenesis has not been fully elucidated. Reactive oxygen species (ROS) play a pivotal role in the progression of CVD. Particularly, ROS are commonly engaged in developing typical characteristics of atherosclerosis, one of the dominant CVDs. This review will discuss the involvement of ROS in atherosclerosis, specifically their effect on inflammation, disturbed blood flow and arterial wall remodeling. Pharmacological interventions target ROS in order to alleviate oxidative stress and CVD symptoms, yet results are varied due to the paradoxical role of ROS in CVD. Lack of effectiveness in clinical trials suggests that understanding the exact role of ROS in the pathophysiology of CVD and developing novel treatments, such as antioxidant gene therapy and nanotechnology-related antioxidant delivery, could provide a therapeutic advance in treating CVDs. While genetic therapies focusing on specific antioxidant expression seem promising in CVD treatments, multiple technological challenges exist precluding its immediate clinical applications.
authors.affiliation: Department of Kinesiology, California State University-Chico, Chico, CA 95929, USA. fhe@csuchico.edu.
authors.forename: Feng
authors.initials: F
authors.lastname: He
authors.affiliation: Molecular Physiology and Rehabilitation Research Lab, Radiologic Sciences and Respiratory Therapy Division, School of Health and Rehabilitation Sciences, the Ohio State University College of Medicine, Columbus, OH 43210, USA. zuo.4@osu.edu.|Interdisciplinary Biophysics Graduate Program, the Ohio State University, Columbus, OH 43210, USA. zuo.4@osu.edu.
authors.forename: Li
authors.initials: L
authors.lastname: Zuo
mesh_terms: D000806:Angiotensin-Converting Enzyme Inhibitors / Q000494:pharmacology / Q000627:therapeutic use; D000818:Animals; D000975:Antioxidants / Q000494:pharmacology / Q000627:therapeutic use; D050197:Atherosclerosis / Q000378:metabolism / Q000473:pathology; D002121:Calcium Channel Blockers / Q000494:pharmacology / Q000627:therapeutic use; D002318:Cardiovascular Diseases / Q000188:drug therapy / Q000209:etiology* / Q000378:metabolism* / Q000473:pathology; D015316:Genetic Therapy; D006801:Humans; D015428:Myocardial Reperfusion Injury / Q000378:metabolism / Q000473:pathology; D010084:Oxidation-Reduction / Q000187:drug effects; D018384:Oxidative Stress / Q000187:drug effects; D017382:Reactive Oxygen Species / Q000378:metabolism*; D012307:Risk Factors; D015398:Signal Transduction / Q000187:drug effects
chemical_list: D000806:Angiotensin-Converting Enzyme Inhibitors; D000975:Antioxidants; D002121:Calcium Channel Blockers; D017382:Reactive Oxygen Species
keywords: antioxidant; atherosclerosis; free radical; reactive oxygen species