title: Diabetes, oxidative stress, molecular mechanism, and cardiovascular disease--an overview.
abstract: In recent years, diabetes and its associated complications have come to represent a major public health concern. It is a complex disease characterized by multiple metabolic derangements and is known to impair cardiac function by disrupting the balance between pro-oxidants and antioxidants at the cellular level. The subsequent generation of reactive oxygen species (ROS) and accompanying oxidative stress are hallmarks of the molecular mechanisms responsible for cardiovascular disease. Among several oxidative stress-mediated mechanisms that have been proposed, ROS-mediated oxidative stress has received the most attention. ROS have been shown to interact with proteins, lipids, and DNA, causing damage to the cellular macromolecules and subsequently, deterioration of cellular function. Induction of thioredoxin-1 (Trx1) gene expression has been demonstrated to protect the diabetic myocardium from dysfunction by reducing oxidative stress and enhancing the expression of heme oxygenase-1 (HO-1) and vascular endothelial growth factor (VEGF). The failure of antioxidants to consistently demonstrate clinical benefit necessitates further investigation of the role of oxidative stress in diabetes-mediated cardiovascular disease.
authors.affiliation: Molecular Cardiology and Angiogenesis Laboratory, Department of Surgery, University of Connecticut Health Center, Farmington Avenue, Farmington, Connecticut, USA.
authors.forename: Vaithinathan
authors.initials: V
authors.lastname: Selvaraju
authors.forename: Mandip
authors.initials: M
authors.lastname: Joshi
authors.forename: Sumanth
authors.initials: S
authors.lastname: Suresh
authors.forename: Juan A
authors.initials: JA
authors.lastname: Sanchez
authors.forename: Nilanjana
authors.initials: N
authors.lastname: Maulik
authors.forename: Gautam
authors.initials: G
authors.lastname: Maulik
mesh_terms: D000818:Animals; D000975:Antioxidants / Q000008:administration & dosage / Q000627:therapeutic use; D002311:Cardiomyopathy, Dilated / Q000188:drug therapy / Q000209:etiology* / Q000276:immunology / Q000378:metabolism; D002312:Cardiomyopathy, Hypertrophic / Q000188:drug therapy / Q000209:etiology* / Q000276:immunology / Q000378:metabolism; D002313:Cardiomyopathy, Restrictive / Q000188:drug therapy / Q000209:etiology* / Q000276:immunology / Q000378:metabolism; D058065:Diabetic Cardiomyopathies / Q000188:drug therapy / Q000209:etiology* / Q000276:immunology / Q000378:metabolism; D051547:Heme Oxygenase-1 / Q000096:biosynthesis / Q000235:genetics; D006801:Humans; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors / Q000008:administration & dosage / Q000627:therapeutic use; D018384:Oxidative Stress / Q000187:drug effects; D017382:Reactive Oxygen Species / Q000378:metabolism; D013879:Thioredoxins / Q000235:genetics; D042461:Vascular Endothelial Growth Factor A / Q000096:biosynthesis / Q000235:genetics
chemical_list: D000975:Antioxidants; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors; D017382:Reactive Oxygen Species; D042461:Vascular Endothelial Growth Factor A; D013879:Thioredoxins; D051547:Heme Oxygenase-1