Neutrophil gelatinase-associated lipocalin as a biomarker of cardiovascular disease: a systematic review.

Neutrophil gelatinase-associated lipocalin as a biomarker of cardiovascular disease: a systematic review.
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DOI:
10.1515/cclm-2012-0307
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发表时间:
2012
影响因子:
6.8
通讯作者:
Devarajan P
Devarajan P
中科院分区:
医学2区
文献类型:
--
作者:
Cruz DN;Gaiao S;Maisel A;Ronco C;Devarajan P

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中性粒细胞明胶酶相关脂质运载蛋白(NGAL)是急性肾损伤(阿基)的生物标志物。最近,在心力衰竭、冠心病和中风中也报道了NGAL水平升高。其他研究表明NGAL在衰竭心肌和动脉粥样硬化斑块中上调。我们的目的是综合目前关于NGAL和心血管疾病(CVD)的证据,并阐明全身NGAL水平在CVD中的预后意义。我们进行了系统的回顾,以确定NGAL和CVD的实验和人体研究。我们排除了专门涉及阿基或肾脏终点的文章。我们确定了22项研究,包括动物和人类数据。NGAL在心脏中高度表达,在衰竭的心肌和心肌炎中都是如此,并且还在动脉粥样硬化斑块中表达。NGAL和基质金属蛋白酶(MMP)-9共定位的区域表现出MMP-9蛋白水解活性增加。在几项但不是所有研究中,全身NGAL水平与肾功能和CVD严重程度相关。全身NGAL水平升高与临床结果之间的相关性(例如,死亡、再次入院),但这些研究对潜在混杂因素的调整有限。有大量文献支持NGAL在CVD的病理生理学中的假定作用,但目前关于全身NGAL水平在CVD管理中的临床效用的数据不足。关于NGAL作为CVD结局预测因子的现有证据非常有限。
Neutrophil gelatinase-associated lipocalin (NGAL) is a biomarker of acute kidney injury (AKI). Recently, elevated NGAL levels have also been reported in heart failure, coronary heart disease, and stroke. Other studies demonstrate that NGAL is upregulated in failing myocardium and in atherosclerotic plaque. Our aim was to synthesize the current evidence on NGAL and cardiovascular disease (CVD), and to clarify the prognostic significance of systemic NGAL levels in CVD. We performed a systematic review to identify experimental and human studies on NGAL and CVD. We excluded articles which specifically dealt with AKI or renal endpoints. We identified 22 studies, including both animal and human data. NGAL is highly expressed in the heart, both in failing myocardium and myocarditis, and is also expressed in atherosclerotic plaques. Areas of co-localization of NGAL and matrix metalloproteinase (MMP)-9 exhibited increased MMP-9 proteolytic activity. Systemic NGAL levels correlated with renal function and severity of CVD in several, but not all, studies. An association between elevated systemic NGAL levels and clinical outcomes (e.g., death, hospital readmissions) were reported in six CVD studies, but these had limited adjustment for potential confounders. There is ample literature to support a putative role of NGAL in the pathophysiology of CVD, but at present there is insufficient data regarding the clinical utility of systemic NGAL levels in the management of CVD. Available evidence regarding NGAL as a predictor of outcomes in CVD is very limited.
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