Impact of Oxidative Stress and Mitochondrial Dysfunction on the Regulation of Brain, Heart, Lung and Vascular Functions

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 2024 | Viewed by 419

Special Issue Editor


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Guest Editor
Division of Clinical Pharmacology, Department of Medicine, Vanderbilt University Medical Center, Nashville, TN 37232, USA
Interests: oxidative stress; endothelial dysfunction; vascular dysfunction; systemic hypertension; pulmonary hypertension; mitochondrial dysfunction
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Special Issue Information

Dear Colleagues,

Redox and mitochondrial pathways play a critical role both in the homeostasis and the pathogenesis of cardiovascular disease, stroke, lung disease, cognitive decline and dementia; these diseases represent enormous healthcare and economic burden for society. Understanding the ethology of these conditions is critical to increase the healthspan of individuals and reduce the rates of morbidity and mortality. Multiple risk factors contribute to these pathological conditions. The old paradigm was to focus on systemic metabolic disorders; however, recent studies indicate that cell-specific mitochondria/metabolic dysregulation in the vascular cells promote pathological conditions independently from systemic alterations. This new paradigm provides novel insight into these pathways, such as accelerated vascular aging and crosstalk between cardiac and neurological conditions.

This Special Issue aims to be a platform where cross-disciplinary efforts addressing the gap of knowledge in this field could be disseminated.

Dr. Anna Dikalova
Guest Editor

Manuscript Submission Information

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Keywords

  • oxidative stress
  • mitochondrial dysfunction
  • cardiovascular disease
  • vascular dysfunction
  • ageing

Published Papers (1 paper)

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Research

13 pages, 2238 KiB  
Article
Vitamin E Attenuates Red-Light-Mediated Vasodilation: The Benefits of a Mild Oxidative Stress
by Agnes Keszler, Dorothee Weihrauch, Brian Lindemer, Grant Broeckel and Nicole L. Lohr
Antioxidants 2024, 13(6), 668; https://doi.org/10.3390/antiox13060668 (registering DOI) - 29 May 2024
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Abstract
Red light (670 nm) energy controls vasodilation via the formation of a transferable endothelium-derived nitric oxide (NO)-precursor-containing substance, its intracellular traffic, and exocytosis. Here we investigated the underlying mechanistic effect of oxidative stress on light-mediated vasodilation by using pressure myography on dissected murine [...] Read more.
Red light (670 nm) energy controls vasodilation via the formation of a transferable endothelium-derived nitric oxide (NO)-precursor-containing substance, its intracellular traffic, and exocytosis. Here we investigated the underlying mechanistic effect of oxidative stress on light-mediated vasodilation by using pressure myography on dissected murine arteries and immunofluorescence on endothelial cells. Treatment with antioxidants Trolox and catalase decreased vessel dilation. In the presence of catalase, a lower number of exosomes were detected in the vessel bath. Light exposure resulted in increased cellular free radical levels. Mitochondrial reactive oxygen species were also more abundant but did not alter cellular ATP production. Red light enhanced the co-localization of late exosome marker CD63 and cellular S-nitrosoprotein to a greater extent than high glucose, suggesting that a mild oxidative stress favors the localization of NO precursor in late exosomes. Exocytosis regulating protein Rab11 was more abundant after irradiation. Our findings conclude that red-light-induced gentle oxidative stress facilitates the dilation of blood vessels, most likely through empowering the traffic of vasodilatory substances. Application of antioxidants disfavors this mechanism. Full article
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