Oxidative Stress in Cardiovascular Diseases and Vascular Pathophysiology

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 August 2025 | Viewed by 1583

Special Issue Editor


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Guest Editor
Department of Biochemistry and Genetics, University of Navarra, 31008 Pamplona, Spain
Interests: oxidative stress; hypertension; atherosclerosis; metabolic disorders; NADPH oxidases; telomere
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Special Issue Information

Dear Colleagues,

Reactive oxygen species (ROS), particularly superoxide anion and hydrogen peroxide, play an essential role in numerous cellular physiological processes by modulating several signaling pathways. In contrast, the overproduction of ROS and/or the impairment of endogenous antioxidant defenses induces an imbalance that ultimately leads to a situation of oxidative stress that is implicated in vascular and metabolic diseases, including hypertension, atherosclerosis and diabetes; these constitute the main risk factors for stroke, myocardial infarction and heart failure. Among other effects, oxidative stress alters gene expression, causes endothelial dysfunction, promotes the remodeling of the extracellular matrix, and exacerbates inflammatory and senescent vascular processes. Vascular oxidant-generating enzymes include NADPH oxidases, xanthine oxidases, lipoxygenases, mitochondrial oxidases, and nitric oxide synthases. We still do not fully understand the underlying mechanisms of oxidative stress and the pathological effects that an increase in ROS production has in cardiovascular tissue. Unravelling these underlying causes is essential to enhancing disease therapy. This Special Issue will focus on the novel mechanisms of oxidative stress, its impact on vascular inflammation and dysfunction, the identification of principal ROS-generating enzymes, with a special focus on the NADPH oxidase family and mitochondria, and the potential benefit of targeting these specific sources of oxidative stress to improve vascular function. We invite you to submit your latest research findings or a review article to this Special Issue.

Prof. Dr. Guillermo Zalba
Guest Editor

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Keywords

  • atherosclerosis
  • diabetes
  • heart failure
  • inflammation
  • myocardial infarction
  • NADPH oxidase
  • oxidative stress
  • reactive oxygen species
  • stroke

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Published Papers (1 paper)

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Research

19 pages, 4657 KiB  
Article
NADPH Oxidase 5 (NOX5) Upregulates MMP-10 Production and Cell Migration in Human Endothelial Cells
by Javier Marqués, Elena Ainzúa, Josune Orbe, María Martínez-Azcona, José Martínez-González and Guillermo Zalba
Antioxidants 2024, 13(10), 1199; https://doi.org/10.3390/antiox13101199 - 3 Oct 2024
Viewed by 1108
Abstract
NADPH oxidases (NOXs) have been described as critical players in vascular remodeling, a mechanism modulated by matrix metalloproteinases. In this study, we describe for the first time the upregulation of MMP-10 through the activation of NOX5 in endothelial cells. In a chronic NOX5 [...] Read more.
NADPH oxidases (NOXs) have been described as critical players in vascular remodeling, a mechanism modulated by matrix metalloproteinases. In this study, we describe for the first time the upregulation of MMP-10 through the activation of NOX5 in endothelial cells. In a chronic NOX5 overexpression model in human endothelial cells, MMP-10 production was measured at different levels: extracellular secretion, gene expression (mRNA and protein levels), and promoter activity. Effects on cell migration were quantified using wound healing assays. NOX5 overexpression increased MMP-10 production, favoring cell migration. In fact, NOX5 and MMP-10 silencing prevented this promigratory effect. We showed that NOX5-mediated MMP-10 upregulation involves the redox-sensitive JNK/AP-1 signaling pathway. All these NOX5-dependent effects were enhanced by angiotensin II (Ang II). Interestingly, MMP-10 protein levels were found to be increased in the hearts of NOX5-expressing mice. In conclusion, we described that NOX5-generated ROS may modulate the MMP-10 expression in endothelial cells, which leads to endothelial cell migration and may play a key role in vascular remodeling. Full article
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