Redox Signaling and Oxidative Stress in Cerebrovascular 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: closed (31 December 2019) | Viewed by 13568

Special Issue Editors


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Guest Editor
Department of Clinical and Biological Sciences, University of Torino, 10043 Orbassano, Italy
Interests: Cerebral Cavernous Malformation (CCM); cerebrovascular diseases; oxidative stress; inflammation; reactive oxygen species; NADPH oxidase; Nrf2; redox signaling; autophagy; endothelial cell; vascular biology; blood–brain barrier

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Guest Editor
Vascular Biology Center, Department of Medicine, Cardiology, Medical College of Georgia at Augusta University, Augusta, GA, USA
Interests: reactive oxygen species; redox signaling; vascular endothelial growth factor; angiogenesis; endothelial cells; peripheral arterial disease; diabetes
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Guest Editor
Department of Physiology, Anatomy & Microbiology, School of Life Sciences, La Trobe University, Melbourne, VIC, Australia
Interests: cardiovascular disease
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Guest Editor
Department of Medicine, Division of Cardiology, Emory University, Atlanta, GA, USA

Special Issue Information

Dear Colleagues,

Cerebrovascular diseases are the second leading cause of death and the main cause of adult long-term disability in developed countries, posing as significant unmet clinical needs, as there are limited therapeutic options for many of these disorders.

Accumulating evidence demonstrates that an interplay between oxidative stress and inflammation contributes significantly to the onset, progression and severity of various cerebrovascular diseases, raising the possibility that the underlying mechanisms are interconnected. Furthermore, studies in patient cohorts suggest that genetic susceptibility factors related to differences in vascular sensitivity to oxidative stress and inflammation contribute to inter-individual differences in disease susceptibility and severity.

This special issue will highlight current knowledge and future prospects on the characterization of the role of oxidative stress and inflammation in blood-brain barrier endothelial dysfunction and cerebrovascular diseases, and the identification of underlying redox-sensitive mechanisms, as well as the development of novel therapeutic strategies, including drug combination and personalized medicine approaches.

In particular, we invite investigators to submit original research articles as well as review articles related to the following topics:

  • Role of oxidative stress and/or inflammation in onset and progression of cerebrovascular diseases
  • Role of oxidative stress and/or inflammation in neurovascular unit dysfunction and blood–brain barrier hyperpermeability
  • Mechanisms underlying the crosstalk between oxidative stress and inflammation in endothelial cells and vascular tissues
  • NADPH oxidases as friends or foes of endothelial cells and the vascular system
  • Role of NADPH oxidases and reactive oxygen species in cerebrovascular physiology and pathology
  • Functional crosstalk between Nrf2 and NF-κB signaling pathways in the regulation of endothelial cell responses to oxidative stress and inflammation
  • Role of autophagy in endothelial cell responses to oxidative stress and inflammation
  • Role of autophagy in cerebrovascular physiology and pathology
  • Genetic susceptibility factors related to differences in vascular sensitivity to oxidative stress and inflammation
  • Biomarkers of oxidative stress and inflammation associated with progression and severity of vascular diseases
  • Innovative antioxidant and drug combination therapies for prevention and treatment of vascular diseases

Prof. Dr. Saverio Francesco Retta
Dr. Lorenza Trabalzini
Prof. Dr. Masuko Ushio-Fukai
Prof. Dr. Chris Sobey
Guest Editors

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Published Papers (2 papers)

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Review

22 pages, 1690 KiB  
Review
Vitamin D Deficiency and the Risk of Cerebrovascular Disease
by Hyun Ah Kim, Andrea Perrelli, Alberto Ragni, Francesca Retta, T. Michael De Silva, Christopher G. Sobey and Saverio Francesco Retta
Antioxidants 2020, 9(4), 327; https://0-doi-org.brum.beds.ac.uk/10.3390/antiox9040327 - 17 Apr 2020
Cited by 60 | Viewed by 9807
Abstract
Vitamin D deficiency has been clearly linked to major chronic diseases associated with oxidative stress, inflammation, and aging, including cardiovascular and neurodegenerative diseases, diabetes, and cancer. In particular, the cardiovascular system appears to be highly sensitive to vitamin D deficiency, as this may [...] Read more.
Vitamin D deficiency has been clearly linked to major chronic diseases associated with oxidative stress, inflammation, and aging, including cardiovascular and neurodegenerative diseases, diabetes, and cancer. In particular, the cardiovascular system appears to be highly sensitive to vitamin D deficiency, as this may result in endothelial dysfunction and vascular defects via multiple mechanisms. Accordingly, recent research developments have led to the proposal that pharmacological interventions targeting either vitamin D deficiency or its key downstream effects, including defective autophagy and abnormal pro-oxidant and pro-inflammatory responses, may be able to limit the onset and severity of major cerebrovascular diseases, such as stroke and cerebrovascular malformations. Here we review the available evidence supporting the role of vitamin D in preventing or limiting the development of these cerebrovascular diseases, which are leading causes of disability and death all over the world. Full article
(This article belongs to the Special Issue Redox Signaling and Oxidative Stress in Cerebrovascular Disease)
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20 pages, 831 KiB  
Review
Dicarbonyl Stress and S-Glutathionylation in Cerebrovascular Diseases: A Focus on Cerebral Cavernous Malformations
by Cinzia Antognelli, Andrea Perrelli, Tatiana Armeni, Vincenzo Nicola Talesa and Saverio Francesco Retta
Antioxidants 2020, 9(2), 124; https://0-doi-org.brum.beds.ac.uk/10.3390/antiox9020124 - 01 Feb 2020
Cited by 22 | Viewed by 3187
Abstract
Dicarbonyl stress is a dysfunctional state consisting in the abnormal accumulation of reactive α-oxaldehydes leading to increased protein modification. In cells, post-translational changes can also occur through S-glutathionylation, a highly conserved oxidative post-translational modification consisting of the formation of a mixed disulfide between [...] Read more.
Dicarbonyl stress is a dysfunctional state consisting in the abnormal accumulation of reactive α-oxaldehydes leading to increased protein modification. In cells, post-translational changes can also occur through S-glutathionylation, a highly conserved oxidative post-translational modification consisting of the formation of a mixed disulfide between glutathione and a protein cysteine residue. This review recapitulates the main findings supporting a role for dicarbonyl stress and S-glutathionylation in the pathogenesis of cerebrovascular diseases, with specific emphasis on cerebral cavernous malformations (CCM), a vascular disease of proven genetic origin that may give rise to various clinical signs and symptoms at any age, including recurrent headaches, seizures, focal neurological deficits, and intracerebral hemorrhage. A possible interplay between dicarbonyl stress and S-glutathionylation in CCM is also discussed. Full article
(This article belongs to the Special Issue Redox Signaling and Oxidative Stress in Cerebrovascular Disease)
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