Arteriosclerosis, thrombosis, and vascular biology
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Arterioscler. Thromb. Vasc. Biol. · Jul 2013
Bile acid receptor TGR5 agonism induces NO production and reduces monocyte adhesion in vascular endothelial cells.
TGR5 is a G-protein-coupled receptor for bile acids. So far, little is known about the function of TGR5 in vascular endothelial cells. ⋯ TGR5 agonism induces NO production via Akt activation and intracellular Ca(2+) increase in vascular endothelial cells, and this function inhibits monocyte adhesion in response to inflammatory stimuli.
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Arterioscler. Thromb. Vasc. Biol. · Jul 2013
Editorial CommentTargeting factor XI to prevent thrombosis.
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Arterioscler. Thromb. Vasc. Biol. · Jun 2013
Comparative StudyInsulin sensitivity and carotid intima-media thickness: relationship between insulin sensitivity and cardiovascular risk study.
Despite a wealth of experimental data in animal models, the independent association of insulin resistance with early carotid atherosclerosis in man has not been demonstrated. ⋯ In young-to-middle aged apparently healthy people, the association of CCA-IMT with insulin sensitivity and its metabolic correlates differs between men and women. Lower insulin sensitivity is associated with higher IMT only in men; this association seems to be mediated by circulating free fatty acids and adipocytokines. In women, CCA-IMT is independently associated with fasting plasma glucose.
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Arterioscler. Thromb. Vasc. Biol. · Apr 2013
Novel role of copper transport protein antioxidant-1 in neointimal formation after vascular injury.
Vascular smooth muscle cell (VSMC) migration is critically important for neointimal formation after vascular injury and atherosclerosis lesion formation. Copper (Cu) chelator inhibits neointimal formation, and we previously demonstrated that Cu transport protein antioxidant-1 (Atox1) is involved in Cu-induced cell growth. However, role of Atox1 in VSMC migration and neointimal formation after vascular injury is unknown. ⋯ Atox1 is involved in neointimal formation after vascular injury through promoting VSMC migration and inflammatory cell recruitment in injured vessels. Thus, Atox1 is a potential therapeutic target for VSMC migration and inflammation-related vascular diseases.
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Arterioscler. Thromb. Vasc. Biol. · Apr 2013
Thioredoxin 1 is essential for sodium sulfide-mediated cardioprotection in the setting of heart failure.
The aim of this study was to determine whether thioredoxin 1 (Trx1) mediates the cardioprotective effects of hydrogen sulfide (H2S) in a model of ischemic-induced heart failure (HF). ⋯ These findings provide novel information that the upregulation of Trx1 by Na2S therapy in the setting of HF sets into motion events, such as the inhibition of apoptosis signaling kinase-1 signaling and histone deacetylase 4 nuclear export, which ultimately leads to the attenuationof left-ventricular remodeling.