Potential Role of Protein Disulfide Isomerase in Metabolic Syndrome-Derived Platelet Hyperactivity

被引:12
|
作者
Gaspar, Renato Simoes [1 ]
Trostchansky, Andres [2 ,3 ,4 ]
de Andrade Paes, Antonio Marcus [1 ,4 ]
机构
[1] Univ Fed Maranhao, Dept Physiol Sci, Lab Expt Physiol, Sao Luis, MA, Brazil
[2] Univ Republica, Dept Bioquim, Montevideo, Uruguay
[3] Univ Republica, Fac Med, Ctr Free Rad & Biomed Res, Montevideo, Uruguay
[4] Univ Fed Maranhao, Hlth Sci Grad Program, Biol & Hlth Sci Ctr, Sao Luis, MA, Brazil
关键词
VASCULAR SMOOTH-MUSCLE; TRANSIENT ISCHEMIC ATTACK; NADPH-OXIDASE; NITRIC-OXIDE; OXIDATIVE STRESS; CARDIOVASCULAR RISK; THROMBUS FORMATION; INSULIN-RECEPTOR; NAD(P)H OXIDASE; ACTIVATION;
D O I
10.1155/2016/2423547
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
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.
引用
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页数:10
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