Special Issue "Oxidative Stress in Cardiovascular Disease 2014"


A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Pathology".

Deadline for manuscript submissions: 31 October 2014

Special Issue Editors

Guest Editor
Dr. Francis J. Miller Jr.
Departments of Internal Medicine and Anatomy and Cell Biology, University of Iowa, Veterans Affairs Medical Center, Iowa City, Iowa, USA
Website: http://www.int-med.uiowa.edu/divisions/cardiology/Directory/FrancisMiller.html
E-Mail: francis-miller@uiowa.edu
Interests: atherosclerosis; reactive oxygen species; oxidative stress; smooth muscle cells; NADPH oxidases; restenosis; redox signaling

Guest Editor
Dr. Gabor Csanyi
Vascular Medicine Institute, E1228-1B BST, University of Pittsburgh, 200 Lothrop Street, Pittsburgh, PA 15261, USA
Website: http://www.vmi.pitt.edu/Csanyi.html
E-Mail: gac22@pitt.edu
Interests: oxidative stress, reactive oxygen species, NADPH oxidase, cardiovascular disease, vascular tone dysfunction, thrombospondins, nitric oxide, prostanoids, and EDHF

Guest Editor
Dr. Grant Drummond
Department of Pharmacology, Monash University, Victoria 3800, Australia
Website: http://www.med.monash.edu.au/pharmacology/staff/grant-drummond.html
E-Mail: grant.drummond@monash.edu

Special Issue Information

Dear Colleagues,

Cardiovascular disease is the leading cause of mortality and the most expensive health condition in the United States. Animal and human data implicate increased levels of reactive oxygen species (ROS) associated with oxidative stress in the pathogenesis of cardiovascular disease. Whereas ROS are essential for normal cellular processes, the molecular effects of increased ROS include the oxidation of DNA, RNA, lipids and proteins resulting in the dysregulation of ion channels, signaling pathways and transcription factors. However, we still do not have a complete understanding of the underlying mechanisms and consequences of increased ROS generation in cardiovascular tissue. Reducing oxidative stress represents a promising approach for prevention and treatment of cardiovascular disease. However, in numerous clinical trials, antioxidant supplementation failed to reduce cardiovascular morbidity or mortality. Therefore, alternative strategies are to achieve targeted delivery of antioxidants or to inhibit specific enzymatic sources of ROS, which include the mitochondria,  NADPH oxidases, xanthine oxidase, lipooxygenase, cyclooxygenase, and nitric oxide synthase. This special issue will focus on the causes and consequence of oxidative stress in cardiovascular disease and explore emerging treatment strategies.

Prof. Dr. Francis Miller, Jr.
Dr. Gabor Csanyi
Dr. Grant Drummond
Guest Editors


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  • oxidative stress, reactive oxygen species
  • heart disease, myocardial infarction, ischemia/reperfusion, preconditioning
  • vascular disease, atherosclerosis, hypertension, restenosis, stroke, thrombosis
  • biomarkers of oxidative stress
  • redox-mediated signaling
  • transcription factors, antioxidant response elements
  • antioxidant therapy

Related Special Issue

Published Papers (3 papers)

by  and
Int. J. Mol. Sci. 2014, 15(7), 11773-11782; doi:10.3390/ijms150711773
Received: 27 May 2014; in revised form: 24 June 2014 / Accepted: 27 June 2014 / Published: 2 July 2014
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abstract graphic

by III and Jr.
Int. J. Mol. Sci. 2014, 15(7), 11324-11349; doi:10.3390/ijms150711324
Received: 9 May 2014; in revised form: 23 May 2014 / Accepted: 6 June 2014 / Published: 25 June 2014
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abstract graphic

by , , , , , ,  and
Int. J. Mol. Sci. 2014, 15(5), 9036-9050; doi:10.3390/ijms15059036
Received: 17 April 2014; in revised form: 12 May 2014 / Accepted: 14 May 2014 / Published: 21 May 2014
Show/Hide Abstract | PDF Full-text (1048 KB) | HTML Full-text | XML Full-text

Last update: 7 August 2014

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