Potential Role of Protein Disulfide Isomerase in Metabolic Syndrome-Derived Platelet Hyperactivity.
Potential Role of Protein Disulfide Isomerase in Metabolic Syndrome-Derived Platelet Hyperactivity.
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DOI：
10.1155/2016/2423547
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发表时间：
2016
影响因子：
--
通讯作者：
Paes AM
中科院分区：
文献类型：
--
作者：
Gaspar RS;Trostchansky A;Paes AM
代谢综合征(METS)已经成为一种世界性的流行病，伴随着高昂的社会经济成本，其诊断标准必须包括以下五个特征中的至少三个：内脏肥胖、高血压、血脂异常、胰岛素抵抗和空腹血糖水平高。METS显示氧化应激增加与血小板过度激活有关，血小板过度激活是METS患者血栓形成和缺血事件的重要组成部分。血小板聚集是由过氧化氢和细胞膜上蛋白质二硫键异构酶(PDI)的活性控制的。PDI氧化还原活性部位存在活性半胱氨酸残基，如在蛋氨酸中观察到的那样，这些残基对血浆氧化状态的变化很敏感。然而，尽管PDI是甲硫氨酸诱导的血小板过度活化的重要途径，如胰岛素抵抗和一氧化氮功能障碍，但对其与甲硫氨酸诱导的血小板过度激活的关系及其代谢特征尚缺乏了解。因此，这篇综述的目的是分析文献中的数据，试图支持PDI在蛋氨酸诱导的血小板过度激活中的可能作用。
Metabolic Syndrome (MetS) has become a worldwide epidemic, alongside with a high socioeconomic cost, and its diagnostic criteria must include at least three out of the five features: visceral obesity, hypertension, dyslipidemia, insulin resistance, and high fasting glucose levels. MetS shows an increased oxidative stress associated with platelet hyperactivation, an essential component for thrombus formation and ischemic events in MetS patients. Platelet aggregation is governed by the peroxide tone and the activity of Protein Disulfide Isomerase (PDI) at the cell membrane. PDI redox active sites present active cysteine residues that can be susceptible to changes in plasma oxidative state, as observed in MetS. However, there is a lack of knowledge about the relationship between PDI and platelet hyperactivation under MetS and its metabolic features, in spite of PDI being a mediator of important pathways implicated in MetS-induced platelet hyperactivation, such as insulin resistance and nitric oxide dysfunction. Thus, the aim of this review is to analyze data available in the literature as an attempt to support a possible role for PDI in MetS-induced platelet hyperactivation.
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DOI：
10.1161/atvbaha.116.307461
发表时间：
2016-06
期刊：
Arteriosclerosis, thrombosis, and vascular biology
影响因子：
--
作者：
Crescente M;Pluthero FG;Li L;Lo RW;Walsh TG;Schenk MP;Holbrook LM;Louriero S;Ali MS;Vaiyapuri S;Falet H;Jones IM;Poole AW;Kahr WH;Gibbins JM
通讯作者：
Gibbins JM
DOI：
10.1161/atvbaha.116.307308
发表时间：
2016-05
期刊：
Arteriosclerosis, thrombosis, and vascular biology
影响因子：
--
作者：
Delaney MK;Kim K;Estevez B;Xu Z;Stojanovic-Terpo A;Shen B;Ushio-Fukai M;Cho J;Du X
通讯作者：
Du X
影响因子：
2.9
作者：
Essex, DW;Miller, A;Feinman, RD
通讯作者：
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影响因子：
4.8
作者：
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通讯作者：
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影响因子：
37.8
作者：
Alberti, K. G. M. M.;Eckel, Robert H.;Smith, Sidney C., Jr.
通讯作者：
Smith, Sidney C., Jr.