Tissue kallikrein-kinin therapy in hypertension and organ damage.

Julie Chao, Grant Bledsoe, Lee Chao
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引用次数: 9

Abstract

Tissue kallikrein is a serine proteinase that cleaves low molecular weight kininogen to produce kinin peptides, which in turn activate kinin receptors to trigger multiple biological functions. In addition to its kinin-releasing activity, tissue kallikrein directly interacts with the kinin B2 receptor, protease-activated receptor-1, and gamma-epithelial Na channel. The tissue kallikrein-kinin system (KKS) elicits a wide spectrum of biological activities, including reducing hypertension, cardiac and renal damage, restenosis, ischemic stroke, and skin wound injury. Both loss-of-function and gain-of-function studies have shown that the KKS plays an important endogenous role in the protection against health pathologies. Tissue kallikrein/kinin treatment attenuates cardiovascular, renal, and brain injury by inhibiting oxidative stress, apoptosis, inflammation, hypertrophy, and fibrosis and promoting angiogenesis and neurogenesis. Approaches that augment tissue kallikrein-kinin activity might provide an effective strategy for the treatment of hypertension and associated organ damage.

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高血压和器官损伤的组织激肽治疗。
组织激肽酶是一种丝氨酸蛋白酶,它能裂解低分子量激肽原产生激肽肽,进而激活激肽受体,触发多种生物功能。除了其激肽释放活性外,组织激肽激酶还直接与激肽B2受体、蛋白酶激活受体-1和γ -上皮Na通道相互作用。组织钾likrein-kinin系统(KKS)具有广泛的生物活性,包括降低高血压、心脏和肾脏损害、再狭窄、缺血性中风和皮肤伤口损伤。功能丧失和功能获得的研究都表明,KKS在预防健康病理方面起着重要的内源性作用。组织激肽激酶/激肽治疗通过抑制氧化应激、细胞凋亡、炎症、肥大和纤维化以及促进血管生成和神经发生来减轻心血管、肾脏和脑损伤。增强组织钾likrein-kinin活性的方法可能为高血压和相关器官损伤的治疗提供有效的策略。
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