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压力超负荷诱导的心肌纤维化动物模型的形态学和功能特征

Morphological and Functional Characteristics of Animal Models of Myocardial Fibrosis Induced by Pressure Overload.

作者信息

Ding Yuejia, Wang Yuan, Jia Qiujin, Wang Xiaoling, Lu Yanmin, Zhang Ao, Lv Shichao, Zhang Junping

机构信息

First Teaching Hospital, Tianjin University of Traditional Chinese Medicine, Tianjin 300193, China.

Qian'an Hospital, Traditional Chinese Medicine, Qian'an 064400, China.

出版信息

Int J Hypertens. 2020 Jan 31;2020:3014693. doi: 10.1155/2020/3014693. eCollection 2020.

DOI:10.1155/2020/3014693
PMID:32099670
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7013318/
Abstract

Myocardial fibrosis is characterized by excessive deposition of myocardial interstitial collagen, abnormal distribution, and excessive proliferation of fibroblasts. According to the researches in recent years, myocardial fibrosis, as the pathological basis of various cardiovascular diseases, has been proven to be a core determinant in ventricular remodeling. Pressure load is one of the causes of myocardial fibrosis. In experimental models of pressure-overload-induced myocardial fibrosis, significant increase in left ventricular parameters such as interventricular septal thickness and left ventricular posterior wall thickness and the decrease of ejection fraction are some of the manifestations of cardiac damage. These morphological and functional changes have a serious impact on the maintenance of physiological functions. Therefore, establishing a suitable myocardial fibrosis model is the basis of its pathogenesis research. This paper will discuss the methods of establishing myocardial fibrosis model and compare the advantages and disadvantages of the models in order to provide a strong basis for establishing a myocardial fibrosis model.

摘要

心肌纤维化的特征是心肌间质胶原过度沉积、分布异常以及成纤维细胞过度增殖。近年来的研究表明,心肌纤维化作为各种心血管疾病的病理基础,已被证明是心室重构的核心决定因素。压力负荷是心肌纤维化的原因之一。在压力超负荷诱导的心肌纤维化实验模型中,左心室参数如室间隔厚度和左心室后壁厚度显著增加以及射血分数降低是心脏损伤的一些表现。这些形态和功能变化对生理功能的维持有严重影响。因此,建立合适的心肌纤维化模型是其发病机制研究的基础。本文将讨论建立心肌纤维化模型的方法,并比较各模型的优缺点,以便为建立心肌纤维化模型提供有力依据。

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本文引用的文献

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Axl expression is increased in early stages of left ventricular remodeling in an animal model with pressure-overload.Axl 表达在压力超负荷动物模型左心室重构早期阶段增加。
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Stachydrine Ameliorates Cardiac Fibrosis Through Inhibition of Angiotensin II/Transformation Growth Factor β1 Fibrogenic Axis.水苏碱通过抑制血管紧张素II/转化生长因子β1纤维化轴改善心脏纤维化。
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Analysis of fibrosis in control or pressure overloaded rat hearts after mechanical unloading by heterotopic heart transplantation.同种异位心脏移植机械卸载后对压力超负荷或对照大鼠心脏纤维化的分析。
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CT-1 (Cardiotrophin-1)-Gal-3 (Galectin-3) Axis in Cardiac Fibrosis and Inflammation.CT-1(心营养素-1)-Gal-3(半乳糖凝集素-3)轴在心纤维化和炎症中的作用。
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