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Cited by 200Nitric Oxide and Endothelin EffectsRedox biology and oxidative stressAntioxidant Activity and Oxidative Stress

The DOI matches its Crossref record; 31 of the 31 references it cites were found in a registry or an index.

Heterozygous Cellular Glutathione Peroxidase Deficiency in the Mouse: Abnormalities in Vascular and Cardiac Function and Structure

Forgione, Marc A., Cap, Andre, Liao, Ronglih, Moldovan, Nicanor I., Eberhardt, Robert T., Lim, Chee Chew, Jones, John, Goldschmidt-Clermont, Pascal J., Loscalzo, Joseph·2002·Circulation
DOI 10.1161/01.cir.0000026820.87824.6a
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Abstract

Background— Oxidant stress has been implicated in the pathogenesis of atherothrombosis and other vascular disorders accompanied by endothelial dysfunction. Glutathione peroxidases (GPx) play an important role in the cellular defense against oxidant stress by utilizing glutathione (GSH) to reduce lipid hydroperoxides and hydrogen peroxide to their corresponding alcohols. Cellular GPx (GPx-1) is the principal intracellular isoform of GPx. We hypothesized that GPx-1 deficiency per se induces endothelial dysfunction and structural vascular abnormalities through increased oxidant stress. Methods and Results— A murine model of heterozygous deficiency of GPx-1 (GPx +/−) was investigated to examine this hypothesis. Mesenteric arterioles in GPx-1 +/− mice demonstrated vasoconstriction to acetylcholine compared with vasodilation in wild-type mice (maximal change in vessel diameter, −13.0±2.8% versus 13.2±2.8%, P <0.0001). We also noted an increase in the plasma and aortic levels of the isoprostane iPF 2α -III, a marker of oxidant stress, in GPx-1 +/− mice compared with wild-type mice (170.4±23 pg/mL plasma versus 98.7±7.1 pg/mL plasma, P <0.03; 11.7±0.87 pg/mg aortic tissue versus 8.2±0.55 pg/mg aortic tissue, P <0.01). Histological sections from the coronary vasculature of GPx-1 +/− mice show increased perivascular matrix deposition, an increase in the number of adventitial fibroblasts, and intimal thickening. These structural abnormalities in the myocardial vasculature were accompanied by diastolic dysfunction after ischemia-reperfusion. Conclusions— These findings demonstrate that heterozygous deficiency of GPx-1 leads to endothelial dysfunction, possibly associated with increased oxidant stress, and to significant structural vascular and cardiac abnormalities. These data illustrate the importance of this key antioxidant enzyme in functional and structural responses of the mammalian cardiovascular system.

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Research works printed but not linked: 11

  1. 10.1161/res.73.1.7685251 · DOI
  2. 1997, J Biol Chem, 272, 10712
  3. 10.1161/hyp.26.3.397 · DOI
  4. 1999, Am J Physiol, 277, H2083
  5. 10.1161/circ.97.19.1930 · DOI
  6. 1998, Gen Physiol Biophys, 17, 71
  7. 10.1161/circ.99.2.224 · DOI
  8. 10.1161/circ.94.1.19 · DOI
  9. 10.1161/atvb.17.11.3230 · DOI
  10. 10.1161/circ.98.25.2822 · DOI
  11. 1996, Circulation, 96, II-216

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Metadata

Authors
Forgione, M. A., Cap, A., Liao, R., Moldovan, N. I., Eberhardt, R. T., Lim, C. C., Jones, J., Goldschmidt-Clermont, P. J., & Loscalzo, J.
Affiliations
  • Boston University (US)
  • From Evans Department of Medicine (M.A.F., R.L., R.T.E., C.C.L., J.L.), Department of Surgery (J.J.), and Whitaker Cardiovascular Institute (M.A.F., A.C., R.L., C.C.L., R.T.E., J.J., J.L.), Boston University School of Medicine, Boston, Mass; Cardiology Section, Department of Medicine (N.M.), The Ohio State University, Columbus, Ohio; and Duke University School of Medicine (P.G.), Durham, NC.
ORCID
Venue
Circulation
Publisher
Ovid Technologies (Wolters Kluwer Health)
Published
2002-08-27
Volume
106
Issue
9
Pages
1154-1158
ISSN
  • 0009-7322 (ISSN-L)
  • 1524-4539
DOI
10.1161/01.cir.0000026820.87824.6a
OpenAlex
W2104128564
Cited by
200
References
31
Citations by year
2026: 2 · 2025: 6 · 2024: 5 · 2023: 1 · 2022: 7 · 2021: 6 · 2020: 4 · 2019: 5 · 2018: 8 · 2017: 10 · 2016: 12 · 2015: 8 · 2014: 8 · 2013: 13 · 2012: 4
FWCI
4.40
Type
journal article
Language
en
Open access
closed
Locations
  • Circulation (publishedVersion)
  • PubMed (publishedVersion)
Funders
  • National Institutes of Health
  • National Heart, Lung, and Blood Institute (HL61795, HL 55993, HL-07224-24, HL58976, R01HL058976, T32HL007224, P50HL055993)
Topics
  • Health Sciences › Medicine › Physiology (medical) › Nitric Oxide and Endothelin Effects
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Redox biology and oxidative stress
  • Health Sciences › Medicine › Biochemistry (medical) › Antioxidant Activity and Oxidative Stress
Keywords
glutathione peroxidase 1, oxidative stress, endothelial dysfunction, atherothrombosis, mesenteric arterioles, acetylcholine-induced vasoconstriction, intimal thickening, myocardial ischemia-reperfusion injury, diastolic dysfunction, antioxidant enzymes, mouse model
MeSH terms
Glutathione Peroxidase GPX1, Animals, Antioxidants, Aorta, Thoracic, Bradykinin, Coronary Vessels, Disease Models, Animal, Dose-Response Relationship, Drug, Glutathione Peroxidase, Cyclic GMP, Heterozygote, Male, Mesentery, Metabolism, Inborn Errors, Microcirculation, Myocardial Contraction, Myocardium, Vasodilator Agents, Vasomotor System, Oxidative Stress, Gene Targeting, Muscarinic Agonists, Nitric Oxide Donors, Mice, In Vitro Techniques

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