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心肌梗死后的血管生成生长因子:批判性评价。

Angiogenic growth factors in myocardial infarction: a critical appraisal.

机构信息

Department of Biological Materials, CSIR - Central Leather Research Institute, Adyar, Chennai, 600020, India.

Department of Food Science and Nutrition, Home Science College and Research Institute, Tamil Nadu Agricultural University, Madurai, 625 014, India.

出版信息

Heart Fail Rev. 2017 Nov;22(6):665-683. doi: 10.1007/s10741-017-9630-7.

DOI:10.1007/s10741-017-9630-7
PMID:28639006
Abstract

In the recent past, substantial advances have been made in the treatment of myocardial infarction (MI). Despite the impact of these positive developments, MI remains to be a leading cause of morbidity as well as mortality. An interesting hypothesis is that the development of new blood vessels (angiogenesis) or the remodeling of preexisting collaterals may form natural bypasses that could compensate for the occlusion of an epicardial coronary artery. A number of angiogenic factors are proven to be elicited during MI. Exogenous supplementation of these growth factors either in the form of recombinant protein or gene would enhance the collateral vessel formation and thereby improve the outcome after MI. The aim of this review is to describe the nature and potentials of different angiogenic factors, their expression, their efficacy in animal studies, and clinical trials pertaining to MI.

摘要

在最近的过去,心肌梗死(MI)的治疗取得了重大进展。尽管这些积极的发展产生了影响,但 MI 仍然是发病率和死亡率的主要原因。一个有趣的假设是,新血管的形成(血管生成)或预先存在的侧支的重塑可能形成自然旁路,以弥补心外膜冠状动脉的闭塞。有许多已证明的血管生成因子在 MI 期间被诱导产生。这些生长因子的外源性补充,无论是重组蛋白的形式还是基因的形式,都可以增强侧支血管的形成,从而改善 MI 后的结果。本文综述的目的是描述不同血管生成因子的性质和潜力、它们的表达、它们在动物研究中的功效以及与 MI 相关的临床试验。

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本文引用的文献

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Cardiac Telocytes in Regeneration of Myocardium After Myocardial Infarction.心肌梗死后心肌再生中的心脏间充质干细胞
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Notch-independent RBPJ controls angiogenesis in the adult heart.Notch 非依赖性 RBPJ 控制成年心脏中的血管生成。
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ERK/HIF-1α/VEGF pathway: a molecular target of ELABELA (ELA) peptide for attenuating cardiac ischemia-reperfusion injury in rats by promoting angiogenesis.ERK/HIF-1α/VEGF 通路:ELABELA(ELA)肽通过促进血管生成减轻大鼠心肌缺血再灌注损伤的分子靶点。
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