Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Pivot Concepts:
Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Target Concepts:
Gene/Protein
Disease
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Drug
Enzyme
Compound
Query: UNIPROT:P47989 (
xanthine oxidase
)
8,633
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
Endothelial dysfunction
represents an imbalance between vasodilatory and vasoconstrictory molecules secreted by endothelium. Oxidative stress is a major factor leading to endothelial dysfunction with significant prognostic implications for cardiovascular events. The generation of reactive oxygen species is strongly related to various oxidase enzymes such as
xanthine oxidase
, uncoupled endothelial nitric oxide synthase, cyclooxygenase, glucose oxidase, lipooxygenase, nicotinamide-adenine dinucleotide phosphate oxidase and to mitochondrial electron transport mechanisms. Several pharmaceutical agents exert effects beyond their principal role, such as anti-inflammatory and antioxidant, while the reports on antioxidant vitamins remain controversial especially those based on large scale studies. Moreover, there are studies on other agents already patented, but these are not well evaluated. Recently, there is growing interest in the role of dietary flavonoids and their potential to improve endothelial function by modifying oxidative stress status. Flavonoids are important components of 'functional foods', with beneficial effects on cardiovascular health, mainly due to their antioxidant activity. However, the vascular-protective role of flavonoids and especially their antioxidant properties are still under investigation.
...
PMID:Antioxidant treatment and endothelial dysfunction: is it time for flavonoids? 2395 9
Endothelial dysfunction
represents a predominant early feature of diabetes, rendering patients with diabetes prone to renal complications, e.g., proteinuria. Recent studies have indicated a possible role for
xanthine oxidase
(XO) in the pathogenesis of vascular dysfunctions associated with diabetes. In the present study, we investigated the contribution of XO activation on the progression of diabetic nephropathy in a mouse model using selective XO inhibitors. Male Ins2
Akita
heterozygous mice were used with wild-type mice as controls. Akita mice were treated with topiroxostat (Topi) or vehicle for 4 wk. Serum uric acid levels were significantly reduced in Akita + Topi mice compared with Akita + vehicle mice. The Akita + Topi group had a significant reduction in urinary albumin excretion compared with the Akita + vehicle group. Mesangial expansion, glomerular collagen type IV deposition, and glomerular endothelial injury (assessed by lectin staining and transmission electron microscopy) were considerably reduced in the Akita + topi group compared with the Akita + vehicle group. Furthermore, glomerular permeability was significantly higher in the Akita + vehicle group compared with the wild-type group. These changes were reduced with the administration of Topi. We conclude that XO inhibitors preserve glomerular endothelial functions and rescue compromised glomerular permeability, suggesting that XO activation plays a vital role in the pathogenesis of diabetic nephropathy.
...
PMID:Non-purine selective xanthine oxidase inhibitor ameliorates glomerular endothelial injury in Ins
Akita
diabetic mice. 3295 51
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