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Macro‐ and microvascular endothelial dysfunction in diabetes

Journal of diabetes, 2017-05, Vol.9 (5), p.434-449 [Peer Reviewed Journal]

2017 Ruijin Hospital, Shanghai Jiaotong University School of Medicine and John Wiley & Sons Australia, Ltd ;2017 Ruijin Hospital, Shanghai Jiaotong University School of Medicine and John Wiley & Sons Australia, Ltd. ;2017 John Wiley & Sons Australia, Ltd and Ruijin Hospital, Shanghai Jiaotong University School of Medicine ;ISSN: 1753-0393 ;EISSN: 1753-0407 ;DOI: 10.1111/1753-0407.12521 ;PMID: 28044409

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  • Title:
    Macro‐ and microvascular endothelial dysfunction in diabetes
  • Author: Shi, Yi ; Vanhoutte, Paul M.
  • Subjects: Animals ; Blood Vessels - physiopathology ; Circulatory system ; Diabetes ; Diabetes Mellitus - physiopathology ; Diabetic Angiopathies - genetics ; Diabetic Angiopathies - metabolism ; Diabetic Angiopathies - physiopathology ; endothelial cells ; Endothelium ; Endothelium, Vascular - physiopathology ; Humans ; MicroRNAs ; MicroRNAs - genetics ; microvasculature ; Microvessels - physiopathology ; miRNA ; nitric oxide ; Nitric Oxide - metabolism ; Oxidative Stress ; 一氧化氮 ; 微循环血管组织 ; 糖尿病 ; 血管内皮细胞
  • Is Part Of: Journal of diabetes, 2017-05, Vol.9 (5), p.434-449
  • Description: Highlights Diabetes affects endothelial function in both large blood vessels and the microvasculature. Diabetes‐induced endothelial dysfunction, especially in the microvasculature, is characterized by reduced nitric oxide (NO) bioavailability, increased oxidative stress, an imbalance between vascular endothelial growth factor (VEGF) and NO, and impairment of endothelial repair. Treatments targeting microRNAs, specifically those interfering with the balance between VEGF and NO and endothelial progenitor cell function, may be promising therapeutic strategies in diabetes. Diabetes reduces endothelium‐dependent relaxations in conduit and resistance arteries. Diabetes‐induced endothelial dysfunction presents itself as a reduced protein expression of endothelial nitric oxide synthase (eNOS), reduced phosphorylation of the active site of the eNOS (i.e. Ser1177; S), increased phosphorylation of its inhibitory site (i.e. Thr495; T), decreased levels of the essential cofactor tetrahydrobiopterin (BH4), enhanced arginase activity, increased levels of asymmetric dimethylarginine (ADMA), and enhanced production of oxygen‐derived free radicals. Initially, prostacyclin (PGI2) and/or endothelium‐dependent hyperpolarization (EDH) take part in compensatory mechanisms when nitric oxide (NO)‐mediated responses are impaired. AA, arachidonic acid; COX, cyclo‐oxygenase; HDL, high‐density lipoprotein; IP, prostacyclin receptor; oxLDL, oxidized low‐density lipoprotein; PGH2, prostaglandin H2; R, receptor; TP, thromboxane receptor. Endothelial cells, as well as their major products nitric oxide (NO) and prostacyclin, play a key role in the regulation of vascular homeostasis. Diabetes mellitus is an important risk factor for cardiovascular disease. Diabetes‐induced endothelial dysfunction is a critical and initiating factor in the genesis of diabetic vascular complications. The present review focuses on both large blood vessels and the microvasculature. The endothelial dysfunction in diabetic macrovascular complications is characterized by reduced NO bioavailability, poorly compensated for by increased production of prostacyclin and/or endothelium‐dependent hyperpolarizations, and increased production or action of endothelium‐derived vasoconstrictors. The endothelial dysfunction of microvascular complications is primarily characterized by decreased release of NO, enhanced oxidative stress, increased production of inflammatory factors, abnormal angiogenesis, and impaired endothelial repair. In addition, non‐coding RNAs (microRNAs) have emerged as participating in numerous cellular processes. Thus, this reviews pays special attention to microRNAs and their modulatory role in diabetes‐induced vascular dysfunction. Some therapeutic strategies for preventing and restoring diabetic endothelial dysfunction are also highlighted. 血管内皮细胞和内皮细胞释放的活性因子是调控血管舒张功能的重要因素。糖尿病是慢性心血管疾病的高危因素之一。目前认为高糖和糖尿病引起的内皮细胞功能障碍是造成血管功能改变,并诱导和加重糖尿病并发症的重要原因。在大血管中(包括传导性和阻抗性动脉),糖尿病诱发的内皮细胞功能障碍表现为一氧化氮生物利用度降低、继发的前列环素产物和内皮细胞依赖性超极化反应代偿不足,以及内皮细胞源性的血管收缩因子产生增加。微循环血管内皮细胞功能障碍主要表现为一氧化氮合成减少、氧化应激反应增加、炎症因子产物增多、血管异常生成和内皮细胞修复功能受损等。非编码RNA是近年来的研究热点,参与细胞的多种功能调节。本文将聚焦于糖尿病引发的血管内皮细胞功能改变,特别关注miRNA在其中的参与和调节作用。在文中最后我们还将讨论一些可能改善或治疗糖尿病内皮细胞功能障碍的方法和策略。
  • Publisher: Melbourne: Wiley Publishing Asia Pty Ltd
  • Language: English
  • Identifier: ISSN: 1753-0393
    EISSN: 1753-0407
    DOI: 10.1111/1753-0407.12521
    PMID: 28044409
  • Source: Journals@Ovid Open Access Journal Collection Rolling
    MEDLINE
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