JAHA:循环氧化还原生物标志物浓度不能改善对2型糖尿病患者不良心血管事件的预测!

2018-02-26 xing.T MedSci原创

由此可见,这些覆盖氧化应激全过程的6个标志物的血浆浓度,与MACE的发生没有显著相关性,与经典危险因素相比,也不能改善2型糖尿病患者的MACE风险识别和分类。

尽管存在病理生理学相关性和有前景的实验数据,但氧化应激生物标记物对心脏风险预测的作用尚不清楚。近日,心血管疾病领域权威杂志JAHA上发表了一篇研究文章。该研究的目的是探讨与已知危险因素不同的氧化应激途径中6种生物标志物在预测2型糖尿病患者心血管不良结局的预测价值。

SURDIAGENE前瞻性队列研究连续纳入了1468例2型糖尿病患者。在基线时对6种标志物进行了检测,记录了平均随访64个月期间的主要心血管不良事件(MACE)-首次发生的心血管死亡、非致命性心肌梗死卒中

在单因素分析中,晚期氧化蛋白产物、氧化溶血抑制试验、缺血修饰白蛋白和血浆总还原能力与MACE风险无关。在单变量分析中,荧光化的晚期糖基化终产物以及羰基化合物与MACE(分别有每变化一SD的风险比=1.38,95%可信区间为1.24‐1.54,P<0.001;每变化一SD的风险比=1.15,95%可信区间为1.04‐1.27,P=0.006),当添加到包含MACE传统危险因素的多变量预测模型中,这些指标并不能显著改善模型的C‐统计量或综合判别指标。

由此可见,这些覆盖氧化应激全过程的6个标志物的血浆浓度,与MACE的发生没有显著相关性,与经典危险因素相比,也不能改善2型糖尿病患者的MACE风险识别和分类。

原始出处:

Maxime Cournot,et al. Circulating Concentrations of Redox Biomarkers Do Not Improve the Prediction of Adverse Cardiovascular Events in Patients With Type 2 Diabetes Mellitus.JAHA.2018. https://doi.org/10.1161/JAHA.117.007397

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createdTime=Wed Feb 28 01:13:00 CST 2018, time=2018-02-28, status=1, ipAttribution=), GetPortalCommentsPageByObjectIdResponse(id=1566723, encodeId=95781566e23ef, content=<a href='/topic/show?id=3c746936567' target=_blank style='color:#2F92EE;'>#生物标志#</a>, beContent=null, objectType=article, channel=null, level=null, likeNumber=28, replyNumber=0, topicName=null, topicId=null, topicList=[TopicDto(id=69365, encryptionId=3c746936567, topicName=生物标志)], attachment=null, authenticateStatus=null, createdAvatar=null, createdBy=63db15173977, createdName=zhu_jun9842, createdTime=Wed Feb 28 01:13:00 CST 2018, time=2018-02-28, status=1, ipAttribution=)]
    2018-03-01 惠映实验室

    学习..谢谢分享.

    0

  5. 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    2018-02-28 zhaohui6731
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Nat commun:在去势难治性前列腺癌中,硫氧还蛋白可以防止雄激素受体诱导的氧化还原损伤

雄激素阻断(AD)治疗失败常常会导致终极的和难治愈的去势难治性前列腺癌(CRPC)。最近,有研究人员展示了氧化还原保护性蛋白-硫氧还蛋白-1(TRX1)随着前列腺癌的恶化以及在雄激素阻断的CRPC细胞中增加,这个现象表明了CRPC对TRX1具有增强的依赖性。研究人员发现,TRX1抑制作用可通过shRNA或者PX-12(在前列腺癌中未测试)来妨碍CRPC细胞的生长,并且比它们相对应的雄激素依赖的物质

Free Radic Biol Med:高脂饮食引起脂肪肝的过程中线粒体氧化还原失衡起了重要作用!

研究提示HFD(高脂肪饮食)促进NAFLD(非酒精性脂肪肝)的机制似乎涉及肝线粒体功能障碍和氧化还原失衡。

Cancer cell:华人科学家发现氧化还原与肺癌新关系

近日,来自中科院生化所和复旦大学的研究人员在国际学术期刊cancer cell在线发表了一项最新研究进展。   LKB1基因能够编码丝氨酸/苏氨酸蛋白激酶LKB1, 研究发现该激酶可以调节细胞能量代谢、抑制生长增殖和维持细胞极性, 而这些都是该基因抑制肿瘤的重要机制。虽然LKB1能够调节细胞生长和能量代谢,但在非小细胞肺癌中,LKB1失活如何协调肿瘤进展与代谢之间的关系仍未可知。