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五聚体蛋白3:一种用于炎症性心血管疾病的新型生物标志物。

Pentraxin 3: a novel biomarker for inflammatory cardiovascular disease.

作者信息

Inoue Kenji, Kodama Tatsuhiko, Daida Hiroyuki

机构信息

Department of Cardiology, Juntendo University Nerima Hospital, Tokyo 177-0033, Japan.

出版信息

Int J Vasc Med. 2012;2012:657025. doi: 10.1155/2012/657025. Epub 2012 Jan 4.

DOI:10.1155/2012/657025
PMID:22347626
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3278926/
Abstract

Numerous studies have recently examined the role of pentraxin 3 (PTX3) in clinical situations. The pentraxin family includes C-reactive protein (CRP); however, unlike CRP, PTX3 is expressed predominantly in atherosclerotic lesions that involve macrophages, neutrophils, dendritic cells, or smooth muscle cells. Interestingly, PTX3 gene expression in human endothelial cells is suppressed to a greater extent by pitavastatin than the expression of 6,000 other human genes that have been examined, suggesting that PTX3 may be a novel biomarker for inflammatory cardiovascular disease. The expression and involvement of PTX3 in cardiovascular diseases are discussed in this paper, along with the characteristics of PTX3 that make it a suitable biomarker; namely, that the physiological concentration is known and it is independent of other risk factors. The results discussed in this paper suggest that further investigations into the potential novel use of PTX3 as a biomarker for inflammatory cardiovascular disease should be undertaken.

摘要

近期有大量研究探讨了五聚体蛋白3(PTX3)在临床中的作用。五聚体蛋白家族包括C反应蛋白(CRP);然而,与CRP不同,PTX3主要在涉及巨噬细胞、中性粒细胞、树突状细胞或平滑肌细胞的动脉粥样硬化病变中表达。有趣的是,与已检测的其他6000个人类基因的表达相比匹伐他汀对人内皮细胞中PTX3基因表达的抑制作用更强,这表明PTX3可能是炎症性心血管疾病的一种新型生物标志物。本文讨论了PTX3在心血管疾病中的表达及作用,以及使其成为合适生物标志物的PTX3的特性;即其生理浓度已知且独立于其他危险因素。本文讨论的结果表明,应进一步研究PTX3作为炎症性心血管疾病生物标志物的潜在新用途。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0669/3278926/75f7763c462d/IJVM2012-657025.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0669/3278926/75f7763c462d/IJVM2012-657025.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0669/3278926/75f7763c462d/IJVM2012-657025.001.jpg

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Soluble TWEAK and PTX3 in nondialysis CKD patients: impact on endothelial dysfunction and cardiovascular outcomes.
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