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心肌细胞来源的β-2 微球蛋白在介导心脏纤维化中的新作用。

Novel role for cardiac myocyte-derived β-2 microglobulin in mediating cardiac fibrosis.

机构信息

Cardiovascular Research Center, Lewis Katz School of Medicine, Temple University, 3500 N. Broad Street, Philadelphia, PA 19140, U.S.A.

出版信息

Clin Sci (Lond). 2018 Oct 5;132(19):2117-2120. doi: 10.1042/CS20180681. Print 2018 Oct 15.

DOI:10.1042/CS20180681
PMID:30291210
Abstract

Hypertension is a significant risk factor for the development of cardiovascular ailments, including ischemic heart disease and diastolic dysfunction. In a recent issue of , Li et al. [ (2018) , 1855-1874] report that β-2 microglobulin (β2M) is a novel secreted soluble factor released by cardiac myocytes during pressure overload that promotes profibrotic gene expression in cardiac fibroblasts both and Their study further identifies elevated β2M levels as a possible biomarker for hypertensive patients with cardiac complications. The authors propose a mechanism that mechanically stretched cardiomyocytes release soluble β2M which, through paracrine communication with cardiac fibroblasts, transactivates epidermal growth factor receptor (EGFR) to initiate acute signal transduction and up-regulate profibrotic genes, thereby promoting fibrosis. Here, we will discuss the background, significance of the study, alternative mechanisms, and future directions.

摘要

高血压是心血管疾病发展的重要危险因素,包括缺血性心脏病和舒张功能障碍。在最近一期的《 》中,Li 等人报告称β-2 微球蛋白(β2M)是心肌细胞在压力超负荷时释放的一种新型分泌可溶性因子,可促进心肌成纤维细胞中致纤维化基因的表达。他们的研究进一步确定了升高的β2M 水平可能是高血压合并心脏并发症患者的生物标志物。作者提出了一种机制,即机械拉伸的心肌细胞释放可溶性β2M,通过与心肌成纤维细胞的旁分泌通讯,激活表皮生长因子受体(EGFR),启动急性信号转导并上调致纤维化基因,从而促进纤维化。在这里,我们将讨论该研究的背景、意义、替代机制和未来方向。

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