Tsumura Suzuki肥胖糖尿病(TSOD)小鼠的纤溶功能低下表型与高血糖无关。

IF 1.9 Q3 PHARMACOLOGY & PHARMACY
Drug Discoveries and Therapeutics Pub Date : 2023-11-18 Epub Date: 2023-10-14 DOI:10.5582/ddt.2023.01064
Naoki Ohkura, Riyo Morimoto-Kamata, Yuichi Kamikubo, Yoshihisa Takahashi, Katsutaka Oishi
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引用次数: 0

摘要

肥胖和糖尿病与动脉血栓形成和静脉血栓栓塞的风险增加有关。Tsumura Suzuki肥胖糖尿病(TSOD)小鼠是阐明这些疾病的分子机制的有用模型。我们研究了血糖正常的[Ng]-TSOD小鼠,其代谢异常伴有凝血和纤溶状态,其表型与标准TSOD小鼠明显不同。与TSOD小鼠一样,抑制纤维蛋白溶解的纤溶酶原激活抑制剂-1(PAI-1)在Ng TSOD小鼠中显著增强,表明它们是低纤溶性的。然而,Ng-TSOD小鼠的凝血参数在正常范围内。这些发现表明,Ng-TSOD小鼠是具有与高血糖无关的低纤溶表型的新型模型。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Hypofibrinolytic phenotype in Tsumura Suzuki Obese Diabetes (TSOD) mice unrelated to hyperglycemia.

Obesity and diabetes mellitus are associated with increased risk of arterial thrombosis and venous thromboembolism. Tsumura Suzuki Obese Diabetes (TSOD) mice are useful models for elucidating the molecular mechanisms of these diseases. We investigated normoglycemic [Ng]-TSOD mice with a metabolic abnormality that was accompanied by a coagulative and fibrinolytic state with a phenotype that distinctly differed from that of standard TSOD mice. As in TSOD mice, plasminogen activation inhibitor-1 (PAI-1) that inhibits fibrinolysis was substantially augmented in Ng-TSOD mice, suggesting that they are hypofibrinolytic. However, blood clotting parameters were within the normal range in Ng-TSOD mice. These findings indicated that Ng-TSOD mice are novel models with a hypofibrinolytic phenotype that is not associated with hyperglycemia.

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来源期刊
Drug Discoveries and Therapeutics
Drug Discoveries and Therapeutics PHARMACOLOGY & PHARMACY-
CiteScore
3.20
自引率
3.20%
发文量
51
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