• 文献检索
  • 文档翻译
  • 深度研究
  • 学术资讯
  • Suppr Zotero 插件Zotero 插件
  • 邀请有礼
  • 套餐&价格
  • 历史记录
应用&插件
Suppr Zotero 插件Zotero 插件浏览器插件Mac 客户端Windows 客户端微信小程序
定价
高级版会员购买积分包购买API积分包
服务
文献检索文档翻译深度研究API 文档MCP 服务
关于我们
关于 Suppr公司介绍联系我们用户协议隐私条款
关注我们

Suppr 超能文献

核心技术专利:CN118964589B侵权必究
粤ICP备2023148730 号-1Suppr @ 2026

文献检索

告别复杂PubMed语法,用中文像聊天一样搜索,搜遍4000万医学文献。AI智能推荐,让科研检索更轻松。

立即免费搜索

文件翻译

保留排版,准确专业,支持PDF/Word/PPT等文件格式,支持 12+语言互译。

免费翻译文档

深度研究

AI帮你快速写综述,25分钟生成高质量综述,智能提取关键信息,辅助科研写作。

立即免费体验

人类心血管疾病、心力衰竭和肥大的动物模型。

Animal models of human cardiovascular disease, heart failure and hypertrophy.

作者信息

Hasenfuss G

机构信息

Abteilung Kardiologie und Pneumologie, Universität Göttingen, Germany.

出版信息

Cardiovasc Res. 1998 Jul;39(1):60-76. doi: 10.1016/s0008-6363(98)00110-2.

DOI:10.1016/s0008-6363(98)00110-2
PMID:9764190
Abstract

The progress made in our understanding of the pathophysiology and treatment of congestive heart failure (CHF) would not have been possible without a number of animal models of heart failure and hypertrophy, each one having unique advantages as well as disadvantages. The species and interventions used to create CHF depends on the scientific question as well as on factors such as ethical and economical considerations, accessibility and reproducibility or the model. How closely the model should mimic the human syndrome of CHF depends on the scientific question under investigation. If the goal is to study pathophysiological processes like remodeling or the function of subcellular systems such as excitation contraction-coupling processes, contractile protein function or energetics, the model of heart failure should mimic the clinical setting as closely as possible. However, if defined causal connections are under investigation such as structure-function analyses or regulation of gene expression, exact reflection of the clinical setting by the animal model may be less important. In this review, animal models of heart failure are discussed with particular focus on similarities between the animal model and the failing human heart regarding myocardial function as well as molecular and subcellular mechanisms. In addition, new models of heart failure and hypertrophy, and finally some recent animal models of myocarditis are reviewed.

摘要

如果没有多种心力衰竭和肥大的动物模型,我们在充血性心力衰竭(CHF)病理生理学和治疗方面取得的进展是不可能实现的,每种模型都有其独特的优缺点。用于创建CHF的物种和干预措施取决于科学问题以及伦理、经济考量、可及性、模型的可重复性等因素。该模型应在多大程度上模拟人类CHF综合征取决于所研究的科学问题。如果目标是研究诸如重塑等病理生理过程或亚细胞系统的功能,如兴奋收缩偶联过程、收缩蛋白功能或能量学,那么心力衰竭模型应尽可能紧密地模拟临床情况。然而,如果正在研究特定的因果关系,如结构-功能分析或基因表达调控,动物模型对临床情况的精确反映可能就没那么重要了。在这篇综述中,我们将讨论心力衰竭的动物模型,特别关注动物模型与衰竭人类心脏在心肌功能以及分子和亚细胞机制方面的相似性。此外,还将综述心力衰竭和肥大的新模型,最后介绍一些最近的心肌炎动物模型。

相似文献

1
Animal models of human cardiovascular disease, heart failure and hypertrophy.人类心血管疾病、心力衰竭和肥大的动物模型。
Cardiovasc Res. 1998 Jul;39(1):60-76. doi: 10.1016/s0008-6363(98)00110-2.
2
Experimental models of heart failure.心力衰竭的实验模型
Cardiovasc Res. 1985 Apr;19(4):181-6. doi: 10.1093/cvr/19.4.181.
3
Subcellular remodeling as a viable target for the treatment of congestive heart failure.亚细胞重塑作为治疗充血性心力衰竭的一个可行靶点。
J Cardiovasc Pharmacol Ther. 2006 Mar;11(1):31-45. doi: 10.1177/107424840601100103.
4
Effects of novel vasopressin receptor antagonists on renal function and cardiac hypertrophy in rats with experimental congestive heart failure.新型血管加压素受体拮抗剂对实验性充血性心力衰竭大鼠肾功能和心脏肥大的影响。
J Pharmacol Exp Ther. 2008 Aug;326(2):414-22. doi: 10.1124/jpet.108.137745. Epub 2008 May 8.
5
Transplantation of Epigenetically Modified Adult Cardiac c-Kit+ Cells Retards Remodeling and Improves Cardiac Function in Ischemic Heart Failure Model.表观遗传修饰的成年心脏c-Kit+细胞移植延缓缺血性心力衰竭模型中的心脏重塑并改善心脏功能
Stem Cells Transl Med. 2015 Sep;4(9):1086-96. doi: 10.5966/sctm.2014-0290. Epub 2015 Aug 3.
6
Characterization of an animal model of postmenopausal cardiac hypertrophy and novel mechanisms responsible for cardiac decompensation using ovariectomized pressure-overloaded rats.绝经后心脏肥厚动物模型的特征及利用去卵巢压力超负荷大鼠探讨心脏失代偿的新机制。
Menopause. 2010 Jan-Feb;17(1):213-21. doi: 10.1097/gme.0b013e3181b57489.
7
RIGHT VENTRICULAR HYPERTROPHY IN ANIMALS AT HIGH ALTITUDE.高海拔地区动物的右心室肥厚
J Appl Physiol. 1963 Sep;18:913-8. doi: 10.1152/jappl.1963.18.5.913.
8
L-type calcium channel abundance and function with cardiac hypertrophy and failure: a review.L型钙通道丰度及功能与心肌肥厚和心力衰竭:综述
J Mol Cell Cardiol. 1998 Oct;30(10):1899-916. doi: 10.1006/jmcc.1998.0755.
9
The potential of sheep for the study of osteopenia: current status and comparison with other animal models.绵羊在骨质疏松症研究中的潜力:现状及与其他动物模型的比较。
Bone. 1995 Apr;16(4 Suppl):277S-284S. doi: 10.1016/8756-3282(95)00026-a.
10
Animal models of primary myocardial diseases.原发性心肌病的动物模型。
Yale J Biol Med. 1980 May-Jun;53(3):191-211.

引用本文的文献

1
Assessment of Contractile and Kinetic Properties of Skeletal and Cardiac Multicellular Preparations in Mouse Models: A Comprehensive Methodological Guide.小鼠模型中骨骼肌和心肌多细胞制剂收缩及动力学特性的评估:综合方法指南
Methods Mol Biol. 2026;2975:263-296. doi: 10.1007/978-1-0716-4811-7_17.
2
Exploring the impact of metformin on testicular aging in Syrian hamsters.
Geroscience. 2025 Sep 20. doi: 10.1007/s11357-025-01871-8.
3
Cell Architecture and Dynamics of Human Induced Pluripotent Stem Cell-Derived Cardiomyocytes (hiPSC-CMs) on Hydrogels with Spatially Patterned Laminin and N-Cadherin.人诱导多能干细胞衍生心肌细胞(hiPSC-CMs)在具有空间图案化层粘连蛋白和N-钙黏蛋白的水凝胶上的细胞结构与动力学
ACS Appl Mater Interfaces. 2025 Jan 8;17(1):174-186. doi: 10.1021/acsami.4c11934. Epub 2024 Dec 16.
4
Renal Inflammation, Oxidative Stress, and Metabolic Abnormalities During the Initial Stages of Hypertension in Spontaneously Hypertensive Rats.自发性高血压大鼠高血压初期的肾脏炎症、氧化应激和代谢异常。
Cells. 2024 Oct 25;13(21):1771. doi: 10.3390/cells13211771.
5
Matricellular protein CCN1 promotes collagen alignment and scar integrity after myocardial infarction.细胞基质蛋白 CCN1 促进心肌梗死后胶原纤维的排列和疤痕的完整性。
Matrix Biol. 2024 Nov;133:14-32. doi: 10.1016/j.matbio.2024.08.001. Epub 2024 Aug 2.
6
Informing Hazard Identification and Risk Characterization of Environmental Chemicals by Combining Transcriptomic and Functional Data from Human-Induced Pluripotent Stem-Cell-Derived Cardiomyocytes.通过整合人诱导多能干细胞衍生心肌细胞的转录组和功能数据,进行环境化学物的危害识别和风险特征描述。
Chem Res Toxicol. 2024 Aug 19;37(8):1428-1444. doi: 10.1021/acs.chemrestox.4c00193. Epub 2024 Jul 24.
7
Optimized New Shengmai Powder modulation of cAMP/Rap1A signaling pathway attenuates myocardial fibrosis in heart failure.优化型新生脉散对cAMP/Rap1A信号通路的调控减轻心力衰竭中的心肌纤维化
Chin Med. 2024 Feb 24;19(1):30. doi: 10.1186/s13020-024-00902-4.
8
Mice, rats, and guinea pigs differ in FMOs expression and tissue concentration of TMAO, a gut bacteria-derived biomarker of cardiovascular and metabolic diseases.在 FMOs 表达和 TMAO(一种源自肠道细菌的心血管和代谢疾病生物标志物)的组织浓度方面,小鼠、大鼠和豚鼠存在差异。
PLoS One. 2024 Jan 24;19(1):e0297474. doi: 10.1371/journal.pone.0297474. eCollection 2024.
9
Crosstalk between fibroblasts and immunocytes in fibrosis: From molecular mechanisms to clinical trials.成纤维细胞与免疫细胞在纤维化中的相互作用:从分子机制到临床试验。
Clin Transl Med. 2024 Jan;14(1):e1545. doi: 10.1002/ctm2.1545.
10
Stem cell therapy for heart failure in the clinics: new perspectives in the era of precision medicine and artificial intelligence.临床心力衰竭的干细胞治疗:精准医学与人工智能时代的新视角。
Front Physiol. 2024 Jan 9;14:1344885. doi: 10.3389/fphys.2023.1344885. eCollection 2023.