Oxidative stress in endothelial cell dysfunction and thrombosis

@article{Loscalzo2002OxidativeSI,
  title={Oxidative stress in endothelial cell dysfunction and thrombosis},
  author={J. Loscalzo},
  journal={Pathophysiology of Haemostasis and Thrombosis},
  year={2002},
  volume={32},
  pages={359 - 360}
}
  • J. Loscalzo
  • Published 2002
  • Medicine, Chemistry
  • Pathophysiology of Haemostasis and Thrombosis
Endothelial dysfunction (ECD) is the earliest phenotypic change in the vasculature following exposure to atherothrombotic risk factors. ECD is associated with decreased synthesis and increased oxidative inactivation of nitric oxide (NO). Critical antioxidant enzymes essential for eliminating reactive oxygen species that can inactivate NO include the superoxide dismutases, the glutathione peroxidases, catalase, and glucose-6-phosphate dehydrogenase. Deficiencies of these enzymes increase… Expand
Angiotensin II, platelets and oxidative stress.
Exogenous thioredoxin reduces inflammation in autoimmune myocarditis.
Endothelium as a Source and Target of H2S to Improve Its Trophism and Function
The enigma of in vivo oxidative stress assessment: isoprostanes as an emerging target
  • S. Basu
  • Medicine
  • Scandinavian Journal of Food & Nutrition
  • 2007
Possible usefulness of apocynin, an NADPH oxidase inhibitor, for nitrate tolerance: prevention of NO donor-induced endothelial cell abnormalities.
Does the oxidation of methionine in thrombomodulin contribute to the hypercoaguable state of smokers and diabetics?
Oxidation of thrombomodulin methionine 388 in cigarette smokers
...
1
2
3
4
...

References

SHOWING 1-9 OF 9 REFERENCES
Antioxidants and atherosclerotic heart disease.
Nitric oxide insufficiency, platelet activation, and arterial thrombosis.
Cellular glutathione peroxidase deficiency and endothelial dysfunction.
Glucose‐6‐phosphate dehydrogenase deficiency promotes endothelial oxidant stress and decreases endothelial nitric oxide bioavailability
Endothelial dysfunction in a murine model of mild hyperhomocyst(e)inemia.
Homocyst(e)ine Decreases Bioavailable Nitric Oxide by a Mechanism Involving Glutathione Peroxidase*
Cellular Redox State and Endothelial Dysfunction in Mildly Hyperhomocysteinemic Cystathionine &bgr;‐Synthase‐Deficient Mice
Plasma glutathione peroxidase deficiency and platelet insensitivity to nitric oxide in children with familial stroke.
Pathophysiol Haemost Thromb
  • Pathophysiol Haemost Thromb
  • 2002