Special Issue "Oxidative Stress in Vascular Disease "

A special issue of Antioxidants (ISSN 2076-3921). This special issue belongs to the section "Health Outcomes of Antioxidants and Oxidative Stress".

Deadline for manuscript submissions: 31 December 2019.

Special Issue Editor

Guest Editor
Prof. Salvatore Santo Signorelli Website E-Mail
Department of Clinic and Experimental Medicine.Medcal Angiology Unit., University of Catania, 95124 Catania, Italy
Interests: peripheral arterial disease; carotid diseases; venous disease; vascular-related chronic disease; inflammation; biomarkers

Special Issue Information

Dear Colleagues,

Oxidative stress theory remains one of the most well-studied and debated topics, particularly with regard to its role in both the promotion and progression of vascular disease. A large number of studies have demonstrated the deleterious effects of activated levels of oxidative stress in chronic inflammation and vascular disease (both arterial and venous). On the other hand, unbalanced or lowered antioxidant capability has also been a subject of focus, with the aim of reducing the detrimental effects of oxidative stress damage. These studies have also led to increased knowledge and the development of innovative approaches in counteracting active oxidative stress. Furthermore, it is crucial to identify both direct and indirect markers of oxidative stress damage. Thus, evaluating the role of oxidative stress on the dysregulation of redox-sensitive biological pathways in vascular diseases is an area of great interest. This Special Issue will publish both review and research articles pertaining to the role of oxidative stress in different types of vascular disease.

Prof. Salvatore Santo Signorelli
Guest Editor

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All papers will be peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Antioxidants is an international peer-reviewed open access monthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 1200 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • oxidative stress
  • biomarkers
  • vascular diseases

Published Papers (2 papers)

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Research

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Open AccessCommunication
Inhibition of Heme Oxygenase Antioxidant Activity Exacerbates Hepatic Steatosis and Fibrosis In Vitro
Antioxidants 2019, 8(8), 277; https://doi.org/10.3390/antiox8080277 - 05 Aug 2019
Abstract
The progression of non-alcoholic fatty liver disease (NAFLD) and the development of hepatic fibrosis is caused by changes in redox balance, leading to an increase of reactive oxygen species (ROS) levels. NAFLD patients are at risk of progressing to non-alcoholic steatohepatitis (NASH), associated [...] Read more.
The progression of non-alcoholic fatty liver disease (NAFLD) and the development of hepatic fibrosis is caused by changes in redox balance, leading to an increase of reactive oxygen species (ROS) levels. NAFLD patients are at risk of progressing to non-alcoholic steatohepatitis (NASH), associated to cardiovascular diseases (CVD), coronary heart disease and stroke. Heme Oxygenase-1 (HO-1) is a potent endogenous antioxidant gene that plays a key role in decreasing oxidative stress. The present work was directed to determine whether use of an inhibitor of HO-1 activity affects lipid metabolism and fibrosis process in hepatic cells. Oil Red assay and mRNA analysis were used to evaluate the triglycerides content and the lipid metabolism pathway in HepG2 cells. ROS measurement, RT-PCR and Soluble collagen assay were used to assess the intracellular oxidant, the fibrosis pathway and the soluble collagen in LX2 cells. The activity of HO-1 was inhibited using Tin Mesoporphyrin IX (SnMP). Our study demonstrates that a non-functional HO system results in an increased lipid storage and collagen release in hepatocytes. Consequently, an increase of HO-1 levels may provide a therapeutic approach to address the metabolic alterations associated with NAFLD and its progression to NASH. Full article
(This article belongs to the Special Issue Oxidative Stress in Vascular Disease )
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Review

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Open AccessReview
Oxidative Stress in Peripheral Arterial Disease (PAD) Mechanism and Biomarkers
Antioxidants 2019, 8(9), 367; https://doi.org/10.3390/antiox8090367 - 02 Sep 2019
Abstract
Hemodynamic dysfunction mainly characterizes pathophysiology of peripheral arterial disease (PAD) leading to chronic ischemia. Hemodynamic dysfunction is the origin of intermittent claudication (chronic PAD) or of critical limb ischemia (very severe PAD). Notably, it is well known that oxidative stress (OxS) plays a [...] Read more.
Hemodynamic dysfunction mainly characterizes pathophysiology of peripheral arterial disease (PAD) leading to chronic ischemia. Hemodynamic dysfunction is the origin of intermittent claudication (chronic PAD) or of critical limb ischemia (very severe PAD). Notably, it is well known that oxidative stress (OxS) plays a pathophysiological role in PAD. The higher production of reactive oxygen species (ROS) from OxS and reduced redox capability are two crucial players in initiating and progressing PAD. A number of biomarkers highlight OxS and monitor it in PAD. The present review summarizes data on OxS, on biomarkers available to mark OxS occurrence and to monitor on PAD progression, as well as to evaluate the effects treatments in PAD patients. In conclusion, by detailing OxS and its biomarkers, we hope to encourage more studies to focus on drugs which combat OxS and inflammation. Full article
(This article belongs to the Special Issue Oxidative Stress in Vascular Disease )
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