Publications by authors named "Kimiyo Murakami"
Reduction of a nitroxyl radical, carbamoyl-PROXYL in association of free radical production and hepatic glutathione (GSH) was investigated in iron overloaded mice using an in vivo L-band electron spin resonance (ESR) spectrometer. Significant increases in hepatic iron, lipid peroxidation and decrease in hepatic GSH were observed in mice intraperitoneally (i.p.
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- Thrombin activates cellular responses like platelet aggregation and smooth muscle cell proliferation via the PAR-1 receptor.
- The study evaluated E5555, a selective thrombin receptor antagonist, showing it effectively inhibits smooth muscle cell proliferation in both lab and rat models.
- E5555 demonstrated potential in reducing neointimal formation after vascular injury and could be beneficial for treating conditions like restenosis and chronic atherothrombotic disease.
Article Synopsis
- Thrombin is a key player in platelet activation through PAR-1, and E5555 has been identified as a potent antagonist of this receptor, effectively blocking thrombin’s action.
- E5555 demonstrates strong inhibition of platelet aggregation induced by thrombin and TRAP in both humans and guinea pigs, but does not affect aggregation caused by ADP or collagen.
- In guinea pig models, E5555 showed significant antithrombotic effects without increasing bleeding time, suggesting its potential as a treatment for atherothrombotic diseases.
Background: Oxidative stress plays an important role in the pathophysiology of heart failure. We determined whether the overexpression of glutathione peroxidase (GSHPx) could attenuate left ventricular (LV) remodeling and failure after myocardial infarction (MI).
Methods And Results: We created MI in 12- to 16-week-old, male GSHPx transgenic mice (TG+MI) and nontransgenic wild-type littermates (WT+MI) by ligating the left coronary artery.