Cited by 133Nitric Oxide and Endothelin EffectsRedox biology and oxidative stressNeutrophil, Myeloperoxidase and Oxidative Mechanisms

Reactive oxygen species and the control of vascular function

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Wolin, Michael S.·2009·American Journal of Physiology-Heart and Circulatory Physiology

Abstract

This article summarizes perspectives on how reactive oxygen species (ROS) and redox signaling mechanisms participate in regulating vascular smooth muscle function that have resulted from our studies over the past 25 years in areas including oxygen sensing and the regulation of cGMP production by soluble guanylate cyclase (sGC) that were presented in the Robert M. Berne Distinguished Lectureship at the 2008 Experimental Biology Meeting. It considers mechanisms controlling the activity of sources of ROS including Nox oxidases and mitochondria by physiological stimuli, vascular diseases processes, and metabolic mechanisms linked to NAD(P)H redox and hypoxia. Metabolic interactions of individual ROS such as hydrogen peroxide with cellular peroxide metabolizing enzymes are viewed as some of the most sensitive ways of influencing cellular signaling systems. The control of cytosolic NADPH redox also seems to be a major contributor to bovine coronary arterial relaxation to hypoxia, where its oxidation functions to coordinate the lowering of intracellular calcium, whereas increased cytosolic NADPH generation in pulmonary arteries appears to maintain elevated Nox oxidase activity, and relaxation to hydrogen peroxide, which is attenuated by hypoxia. The sensitivity of sGC to nitric oxide seems to be regulated by thiol and heme redox systems controlled by cytosolic NADPH. Heme biosynthesis and metabolism are also important factors regulating the sGC system. The signaling pathways controlling oxidases and their colocalization with redox-regulated systems enables selective activation of numerous regulatory mechanisms influencing vascular function in physiological processes and the progression of aging-associated vascular diseases.

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Crossref · 10.1152/ajpheart.01167.2008

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  • Post-prandial hyperglycemia initiates a shift in redox systems, characterized by cellular membrane injury by free radicals, as well as reduced circulating homocysteine levels.

    “It has been proposed that post-prandial hyperglycemia initiates a shift in redox systems, characterized by cellular membrane injury by free radicals, as well as reduced circulating homocysteine levels [56].”

    From Cytoprotective Effects of Hydrogen Sulfide in Novel Rat Models of Non-Erosive Esophagitis (2014) · cites this paper as [56]

    The passage labeled Abstract (page unavailable) says elevated glucose can increase reactive oxygen species in the vessel wall, and the glucose-metabolism passage links glucose pathways to cellular redox control. It does not establish the specifically post-prandial setting, free-radical injury to cell membranes, or reduced circulating homocysteine; searches for those terms did not find supporting passages. (LLM, conf=0.86)

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Authors
Wolin, M. S.
Affiliations
New York Medical College (US)
Corresponding author
Wolin, Michael S.
Venue
American Journal of Physiology-Heart and Circulatory Physiology
Published
2009-03
Volume
296
Issue
3
Pages
H539-H549
ISSN
  • 0363-6135 (ISSN-L)
  • 1522-1539
OpenAlex
W2144920190
Cited by
133
References
80
Citations by year
2026: 1 · 2024: 6 · 2022: 2 · 2021: 3 · 2020: 2 · 2019: 4 · 2018: 5 · 2017: 5 · 2016: 8 · 2015: 9 · 2014: 9 · 2013: 20 · 2012: 12
FWCI
13.03
Type
journal article
Language
en
Open access
Locations
  • American Journal of Physiology-Heart and Circulatory Physiology (publishedVersion)
  • PubMed Central (publishedVersion)
  • PubMed (publishedVersion)
Funders
National Heart, Lung, and Blood Institute (P01HL043023, HL 66331, R01HL066331, HL 43023, HL-31069, R01HL031069)
Topics
  • Health Sciences › Medicine › Physiology › Nitric Oxide and Endothelin Effects
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Redox biology and oxidative stress
  • Life Sciences › Immunology and Microbiology › Immunology › Neutrophil, Myeloperoxidase and Oxidative Mechanisms
Keywords
reactive oxygen species, redox signaling, vascular smooth muscle, soluble guanylate cyclase, cyclic GMP, NAD(P)H, NADPH oxidase, mitochondria, oxygen sensing, hypoxia, hydrogen peroxide, nitric oxide, heme biosynthesis, vasorelaxation, coronary arteries, pulmonary artery
MeSH terms
Aging, Animals, Hypoxia, Calcium, Cyclic GMP, Guanylate Cyclase, Heme Oxygenase (Decyclizing), Humans, Mitochondria, Muscle, Muscle, Smooth, Vascular, Nitric Oxide, Oxidation-Reduction, Vascular Diseases, Vasoconstriction, Vasodilation, Signal Transduction, Reactive Oxygen Species, NADPH Oxidases

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