摘要
糖尿病性视网膜病变(DR)是主要的糖尿病并发症,是成年人群视力丧失和失明的主要原因。作为内分泌障碍的糖尿病会紊乱许多荷尔蒙系统,包括肾素血管紧张素系统(RAS),从而可能损害视网膜中的血管和神经元细胞。血管紧张素II(Ang II)是RAS的活性成分在糖尿病视网膜中增加,并且可能在导致DR进展的神经血管损伤中起重要作用。在这篇综述文章中,我们强调了Ang II在糖尿病视网膜损伤的发病机制中的作用,并讨论了一种新发现的机制,涉及组织糜酶和血管紧张素(1-12)[Ang-(1-12)]途径。我们还讨论了靶向阻断细胞Ang II形成以预防/保护视网膜损伤的潜在RAS抑制剂的治疗效果。因此,更好地了解糖尿病视网膜中Ang II形成途径将阐明视力丧失的早期分子机制。这些概念可能提供预防和/或治疗糖尿病视网膜病变的新颖策略,这是全球失明的主要原因。
关键词: 血管紧张素II,食糜酶,糖尿病性视网膜病变,神经变性,氧化应激,肾素 - 血管紧张素系统,视网膜。
Current Medicinal Chemistry
Title:Role of Tissue Renin-angiotensin System and the Chymase/angiotensin-( 1-12) Axis in the Pathogenesis of Diabetic Retinopathy
Volume: 24 Issue: 28
关键词: 血管紧张素II,食糜酶,糖尿病性视网膜病变,神经变性,氧化应激,肾素 - 血管紧张素系统,视网膜。
摘要: Diabetic retinopathy (DR) is a major diabetes complication and the leading cause for vision loss and blindness in the adult human population. Diabetes, being an endocrinological disorder dysregulates a number of hormonal systems including the renin angiotensin system (RAS), which thereby may damage both vascular and neuronal cells in the retina. Angiotensin II (Ang II), an active component of the RAS is increased in diabetic retina, and may play a significant role in neurovascular damage leading to the progression of DR. In this review article, we highlight the role of Ang II in the pathogenesis of retinal damage in diabetes and discuss a newly identified mechanism involving tissue chymase and angiotensin-(1-12) [Ang-(1-12)] pathways. We also discuss the therapeutic effects of potential RAS inhibitors targeting blockade of cellular Ang II formation to prevent/ protect the retinal damage. Thus, a better understanding of Ang II formation pathways in the diabetic retina will elucidate early molecular mechanism of vision loss. These concepts may provide a novel strategy for preventing and/or treating diabetic retinopathy, a leading cause of blindness worldwide.
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Cite this article as:
Role of Tissue Renin-angiotensin System and the Chymase/angiotensin-( 1-12) Axis in the Pathogenesis of Diabetic Retinopathy, Current Medicinal Chemistry 2017; 24 (28) . https://dx.doi.org/10.2174/0929867324666170407141955
DOI https://dx.doi.org/10.2174/0929867324666170407141955 |
Print ISSN 0929-8673 |
Publisher Name Bentham Science Publisher |
Online ISSN 1875-533X |
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