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首页> 外文期刊>Biological chemistry >Kallikrein(K1)-kinin-kininase (ACE) and end-organ damage in ischemia and diabetes: therapeutic implications
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Kallikrein(K1)-kinin-kininase (ACE) and end-organ damage in ischemia and diabetes: therapeutic implications

机译:激肽释放酶(K1)-激肽激肽酶(ACE)与缺血和糖尿病中的终末器官损害:治疗意义

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摘要

Genetic and pharmacological studies, clinical and experimental, focused on kallikrein-K1, kinin receptors and ACE/kininase II suggest that kinin release in the settings of ischemia or diabetes reduces organ damage, especially in the heart and kidney. Kinin bioavailability may be a limiting factor for efficacy of current kinin-potentiating drugs, like ACE inhibitors. Primary activation of kinin receptors by prototypic pharmacological agonists, peptidase-resistant, selective B1 or B2, displays therapeutic efficacy in experimental cardiac and peripheral ischemic and diabetic diseases. B1R agonism was especially efficient in diabetic animals and had no unwanted effects. Clinical development of kinin receptor agonists may be warranted.
机译:针对激肽释放酶-K1,激肽受体和ACE /激肽酶II的遗传和药理学研究(无论是临床还是实验性研究)表明,缺血或糖尿病患者中激肽释放可减少器官损害,尤其是在心脏和肾脏中。激肽的生物利用度可能是当前激肽增强药物(如ACE抑制剂)功效的限制因素。原型药理激动剂对肽激酶的抵抗,选择性的B1或B2对激肽受体的初步激活在实验性心脏和外周缺血性和糖尿病性疾病中显示出治疗功效。 B1R激动剂在糖尿病动物中特别有效,并且没有不良影响。激肽受体激动剂的临床开发可能是必要的。

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