Emerging roles of thiol oxidoreductase-dependent mechanisms on vasomotricity regulation

IF 2.7
Carolina Morales Portas , Geovana Stefani Garcia , Renato Simões Gaspar , Annelise da Silva Casagrande, Leonardo Yuji Tanaka
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引用次数: 1

Abstract

Vasomotricity, defined by measurements of contraction or relaxation, is important to support correct blood supply and needs to be finely regulated during hemodynamic changes. Disruptions in either contraction or relaxation, mainly endothelium-mediated, are closely related to cardiovascular diseases and are found during early events of vascular structural alterations, including vessel remodeling. Both acute vasomotor changes and chronic vascular remodeling are regulated by redox processes, such as the production of nitric oxide (NO), which is the major vasoactive endothelium-derived paracrine molecule. However, it is still unclear if vasomotricity can be regulated by direct redox reactions or thiol posttranslational modifications induced by secondary mediators. Here, we have reviewed the literature concerning the control of vascular function based on redox processes and merged evidence with mechanisms supporting structural alterations. Such knowledge is important to summarize the resulting vascular effects that occur upon inhibition of specific redox regulators. This may provide a landscape to better understand the complex redox regulation of vasomotricity and determine a hierarchical map of events involving NO biology, calcium transient regulation, actin cytoskeleton and extracellular matrix organization. In addition, we have proposed that the thiol oxidoreductase protein disulfide isomerase A1 (PDI) has the potential to act as a central hub connecting these processes with local oxidant generation, which may globally impact vascular function in physiologic and pathologic processes. Altogether, the understanding of these redox processes may lead to potential therapeutic redox targets able to prevent or treat functional or structural vascular alterations.

巯基氧化还原酶依赖性机制在血管舒张性调节中的新作用
血管舒张性,通过测量收缩或舒张来定义,对于支持正确的血液供应是重要的,需要在血流动力学变化期间进行精细调节。收缩或舒张的中断,主要是内皮介导的,与心血管疾病密切相关,并在血管结构改变(包括血管重塑)的早期事件中发现。急性血管舒缩变化和慢性血管重构均受氧化还原过程的调节,如一氧化氮(NO)的产生,一氧化氮是主要的血管活性内皮源旁分泌分子。然而,尚不清楚血管收缩性是否可以通过直接氧化还原反应或由二级介质诱导的巯基翻译后修饰来调节。在此,我们回顾了有关氧化还原过程控制血管功能的文献,并将证据与支持结构改变的机制合并在一起。这些知识对于总结抑制特定氧化还原调节剂所产生的血管效应是很重要的。这可能为更好地理解血管收缩性的复杂氧化还原调节提供了一个视角,并确定了涉及NO生物学、钙瞬态调节、肌动蛋白细胞骨架和细胞外基质组织的事件的层次图。此外,我们还提出硫醇氧化还原酶蛋白二硫异构酶A1 (PDI)有可能作为连接这些过程和局部氧化剂生成的中心枢纽,这可能在生理和病理过程中全面影响血管功能。总之,对这些氧化还原过程的理解可能会导致能够预防或治疗功能或结构血管改变的潜在治疗氧化还原靶点。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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来源期刊
CiteScore
2.60
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0.00%
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审稿时长
46 days
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