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细胞外基质与心血管病理生理学

Extracellular matrix in cardiovascular pathophysiology.

机构信息

Department of Cardiovascular and Renal Research, Institute of Molecular Medicine, University of Southern Denmark.

Mississippi Center for Heart Research, Department of Physiology and Biophysics, University of Mississippi Medical Center , Jackson, Mississippi.

出版信息

Am J Physiol Heart Circ Physiol. 2018 Dec 1;315(6):H1687-H1690. doi: 10.1152/ajpheart.00631.2018. Epub 2018 Sep 21.

DOI:10.1152/ajpheart.00631.2018
PMID:30239231
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6336969/
Abstract

The extracellular matrix (ECM) actively participates in diverse aspects of cardiovascular development and physiology as well as during disease development and progression. ECM roles are determined by its physical and mechanical properties and by its capacity to both release bioactive signals and activate cell signaling pathways. The ECM serves as a storage depot for a wide variety of molecules released in response to injury or with aging. Indeed, there is a plethora of examples describing how cells react to or modify ECM stiffness, how cells initiate intracellular signaling pathways, and how cells respond to the ECM. This Perspectives article reviews the contributions of 21 articles published in the American Journal of Physiology-Heart and Circulatory Physiology in response to a Call for Papers on this topic. Here, we summarize the contributions of these studies focused on the cardiac and vascular ECM. We highlight the translational importance of these studies and conclude that the ECM is a critical component of both the heart and vasculature. Readers are urged to examine and learn from this special Call for Papers.

摘要

细胞外基质(ECM)积极参与心血管发育和生理学的各个方面,以及在疾病发展和进展过程中。ECM 的作用取决于其物理和机械特性,以及其释放生物活性信号和激活细胞信号通路的能力。ECM 是多种在受伤或衰老时释放的分子的储存库。事实上,有很多例子描述了细胞如何对 ECM 硬度做出反应或进行修饰,细胞如何启动细胞内信号通路,以及细胞如何对 ECM 做出反应。这篇观点文章回顾了美国生理学杂志——心脏和循环生理学上发表的 21 篇回应这一主题的论文。在这里,我们总结了这些专注于心脏和血管 ECM 的研究的贡献。我们强调了这些研究的转化重要性,并得出结论,ECM 是心脏和血管的关键组成部分。我们敦促读者研究并学习这一特别的论文征集。

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本文引用的文献

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Temporal changes in myocardial collagen, matrix metalloproteinases, and their tissue inhibitors in the left ventricular myocardium in experimental chronic mitral regurgitation in rodents.实验性慢性鼠二尖瓣反流中左心室心肌胶原、基质金属蛋白酶及其组织抑制剂的时间变化。
Am J Physiol Heart Circ Physiol. 2018 Nov 1;315(5):H1269-H1278. doi: 10.1152/ajpheart.00099.2018. Epub 2018 Aug 24.
2
Surgical reinforcement alters collagen alignment and turnover in healing myocardial infarcts.外科加强治疗改变愈合心肌梗死中的胶原排列和转换。
Am J Physiol Heart Circ Physiol. 2018 Oct 1;315(4):H1041-H1050. doi: 10.1152/ajpheart.00088.2018. Epub 2018 Jul 20.
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Statistical considerations in reporting cardiovascular research.报告心血管研究的统计学考虑因素。
Am J Physiol Heart Circ Physiol. 2018 Aug 1;315(2):H303-H313. doi: 10.1152/ajpheart.00309.2018. Epub 2018 Jul 20.
4
Chronic treatment with the mitochondrial peptide humanin prevents age-related myocardial fibrosis in mice.慢性给予线粒体肽人促胰岛素可预防小鼠与年龄相关的心肌纤维化。
Am J Physiol Heart Circ Physiol. 2018 Nov 1;315(5):H1127-H1136. doi: 10.1152/ajpheart.00685.2017. Epub 2018 Jul 13.
5
Proteomics reveals Rictor as a noncanonical TGF-β signaling target during aneurysm progression in Marfan mice.蛋白质组学揭示了 Rictor 在马凡氏综合征小鼠动脉瘤进展过程中作为非经典 TGF-β 信号靶点的作用。
Am J Physiol Heart Circ Physiol. 2018 Nov 1;315(5):H1112-H1126. doi: 10.1152/ajpheart.00089.2018. Epub 2018 Jul 13.
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Delivery of a matrix metalloproteinase-responsive hydrogel releasing TIMP-3 after myocardial infarction: effects on left ventricular remodeling.心肌梗死后递送基质金属蛋白酶响应水凝胶释放 TIMP-3:对左心室重构的影响。
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Antifibrotic cardioprotection of berberine via downregulating myocardial IGF-1 receptor-regulated MMP-2/MMP-9 expression in diabetic rats.小檗碱通过下调糖尿病大鼠心肌 IGF-1 受体调节的 MMP-2/MMP-9 表达发挥抗纤维化心脏保护作用。
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