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首页> 外文期刊>Seminars in ophthalmology >The Role of Plasma Kallikrein-Kinin Pathway in the Development of Diabetic Retinopathy: Pathophysiology and Therapeutic Approaches
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The Role of Plasma Kallikrein-Kinin Pathway in the Development of Diabetic Retinopathy: Pathophysiology and Therapeutic Approaches

机译：血浆激肽释放酶-激肽通路在糖尿病性视网膜病变发展中的作用：病理生理学和治疗方法

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Diabetic retinal disease is characterized by a series of retinal microvascular changes and increases in retinal vascular permeability that lead to development of diabetic retinopathy (DR) and diabetic macular edema (DME), respectively. Current treatment strategies for DR and DME are mostly limited to vascular endothelial growth factor (VEGF) inhibitors and laser photocoagulation. These treatment modalities are not universally effective in all patients, and potential side effects persist in a significant portion of patients. The plasma kallikrein-kinin system (KKS) is one of the pathways that has been identified in the vitreous in proliferative DR and DME. Preclinical studies have shown that the activation of intraocular KKS induces retinal vascular permeability, vasodilation, and retinal thickening. Proteomic analysis from vitreous of eyes with DME has shown that KKS and VEGF pathways are potentially independent biologic pathways. Furthermore, proteins associated with DME in the vitreous were significantly more correlated with the KKS pathway compared to VEGF pathway. Preclinical experiments on diabetic animals showed that inhibition of KKS components was found to be an effective approach to decrease retinal vascular permeability. An initial phase I human trial of a novel plasma kallikrein inhibitor for the treatment of DME is currently ongoing to test the safety of this approach and serves as an initial step in the translation of basic science discovery into an innovative clinical intervention.
机译：糖尿病性视网膜疾病的特征在于一系列的视网膜微血管变化和视网膜血管通透性的增加，分别导致糖尿病性视网膜病（DR）和糖尿病性黄斑水肿（DME）的发展。 DR和DME的当前治疗策略主要限于血管内皮生长因子（VEGF）抑制剂和激光光凝。这些治疗方式并非对所有患者都普遍有效，并且潜在的副作用在很大一部分患者中仍然存在。血浆激肽释放酶激肽系统（KKS）是玻璃体中增殖性DR和DME中已确定的途径之一。临床前研究表明，眼内KKS的激活可引起视网膜血管通透性，血管舒张和视网膜增厚。用DME对眼玻璃体进行的蛋白质组学分析表明，KKS和VEGF途径是潜在的独立生物学途径。此外，与VEGF途径相比，玻璃体中与DME相关的蛋白质与KKS途径的相关性更高。对糖尿病动物的临床前实验表明，抑制KKS成分是降低视网膜血管通透性的有效方法。目前正在进行一种新型血浆激肽释放酶抑制剂治疗DME的第一阶段人体试验，以测试这种方法的安全性，并且是将基础科学发现转化为创新性临床干预措施的第一步。

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