• 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

一种用于研究全小鼠心脏心肌纤维化的新型体外模型。

A New Ex Vivo Model to Study Cardiac Fibrosis in Whole Mouse Hearts.

作者信息

Kruithof Boudewijn P T, Mousavi Gourabi Babak, van de Merbel Arjanneke F, DeRuiter Marco C, Goumans Marie-José

机构信息

Department of Cardiology, Leiden University Medical Center, Leiden, the Netherlands.

Department of Cell and Chemical Biology, Leiden University Medical Center, Leiden, the Netherlands.

出版信息

JACC Basic Transl Sci. 2024 Jul 31;9(8):1005-1022. doi: 10.1016/j.jacbts.2024.04.007. eCollection 2024 Aug.

DOI:10.1016/j.jacbts.2024.04.007
PMID:39297130
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11405901/
Abstract

Fibrosis is a characteristic of many cardiac diseases for which no effective treatment exists. We have developed an ex vivo flow system, which allows induction of cardiac fibrosis in intact adult mouse hearts. Lineage-tracing studies indicated that the collagen-producing myofibroblasts originated from the resident fibroblasts. The extent of fibrosis was flow rate dependent, and pharmacological inhibition of the transforming growth factor beta signaling pathway prevented fibrosis. Therefore, in this powerful system, the cellular and molecular mechanisms underlying cardiac fibrosis can be studied. In addition, new targets can be tested on organ level for their ability to inhibit fibrosis.

摘要

纤维化是许多心脏病的一个特征，目前尚无有效的治疗方法。我们开发了一种体外流动系统，可在完整的成年小鼠心脏中诱导心脏纤维化。谱系追踪研究表明，产生胶原蛋白的肌成纤维细胞起源于驻留的成纤维细胞。纤维化程度取决于流速，转化生长因子β信号通路的药理学抑制可预防纤维化。因此，在这个强大的系统中，可以研究心脏纤维化的细胞和分子机制。此外，新的靶点可以在器官水平上测试其抑制纤维化的能力。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3e31/11405901/ba9436ea6f28/gr7.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3e31/11405901/d4919f832363/ga1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3e31/11405901/85adf8c76f60/gr1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3e31/11405901/77149c091799/gr2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3e31/11405901/69de94a35836/gr3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3e31/11405901/4c1f3badb588/gr4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3e31/11405901/ad1e89e59e9c/gr5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3e31/11405901/1303bca918f9/gr6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3e31/11405901/ba9436ea6f28/gr7.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3e31/11405901/d4919f832363/ga1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3e31/11405901/85adf8c76f60/gr1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3e31/11405901/77149c091799/gr2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3e31/11405901/69de94a35836/gr3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3e31/11405901/4c1f3badb588/gr4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3e31/11405901/ad1e89e59e9c/gr5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3e31/11405901/1303bca918f9/gr6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3e31/11405901/ba9436ea6f28/gr7.jpg

相似文献

1
A New Ex Vivo Model to Study Cardiac Fibrosis in Whole Mouse Hearts.一种用于研究全小鼠心脏心肌纤维化的新型体外模型。
JACC Basic Transl Sci. 2024 Jul 31;9(8):1005-1022. doi: 10.1016/j.jacbts.2024.04.007. eCollection 2024 Aug.
2
Featured Article: TGF-β1 dominates extracellular matrix rigidity for inducing differentiation of human cardiac fibroblasts to myofibroblasts.特色文章：TGF-β1 通过控制细胞外基质硬度诱导人心肌成纤维细胞分化为肌成纤维细胞。
Exp Biol Med (Maywood). 2018 Apr;243(7):601-612. doi: 10.1177/1535370218761628. Epub 2018 Mar 4.
3
HuR-dependent expression of Wisp1 is necessary for TGFβ-induced cardiac myofibroblast activity.HuR 依赖性表达 Wisp1 对于 TGFβ 诱导的心肌成纤维细胞活性是必需的。
J Mol Cell Cardiol. 2023 Jan;174:38-46. doi: 10.1016/j.yjmcc.2022.10.007. Epub 2022 Nov 11.
4
Glutamyl-Prolyl-tRNA Synthetase Regulates Proline-Rich Pro-Fibrotic Protein Synthesis During Cardiac Fibrosis.谷氨酰 - 脯氨酰 -tRNA 合成酶在心脏纤维化过程中调节富含脯氨酸的促纤维化蛋白的合成。
Circ Res. 2020 Aug 28;127(6):827-846. doi: 10.1161/CIRCRESAHA.119.315999. Epub 2020 Jul 1.
5
MicroRNA‑331 inhibits isoproterenol‑induced expression of profibrotic genes in cardiac myofibroblasts via the TGFβ/smad3 signaling pathway.微小 RNA-331 通过 TGFβ/smad3 信号通路抑制异丙肾上腺素诱导的心肌成纤维细胞中纤维生成基因的表达。
Sci Rep. 2021 Jan 28;11(1):2548. doi: 10.1038/s41598-021-82226-z.
6
Apilimod alters TGFβ signaling pathway and prevents cardiac fibrotic remodeling.阿匹利莫德改变转化生长因子β信号通路并预防心脏纤维化重塑。
Theranostics. 2021 Apr 19;11(13):6491-6506. doi: 10.7150/thno.55821. eCollection 2021.
7
Transforming growth factor-β-dependent Wnt secretion controls myofibroblast formation and myocardial fibrosis progression in experimental autoimmune myocarditis.转化生长因子-β 依赖性 Wnt 分泌控制实验性自身免疫性心肌炎中的成肌纤维细胞形成和心肌纤维化进展。
Eur Heart J. 2017 May 7;38(18):1413-1425. doi: 10.1093/eurheartj/ehw116.
8
Inhibition of transforming growth factor β1 signaling in resident interstitial cells attenuates profibrotic gene expression and preserves erythropoietin production during experimental kidney fibrosis in mice.抑制驻留间质细胞中的转化生长因子β1信号传导可减弱促纤维化基因表达，并在小鼠实验性肾纤维化过程中维持促红细胞生成素的产生。
Kidney Int. 2021 Jul;100(1):122-137. doi: 10.1016/j.kint.2021.02.035. Epub 2021 Mar 9.
9
Apelin prevents cardiac fibroblast activation and collagen production through inhibition of sphingosine kinase 1.Apelin 通过抑制鞘氨醇激酶 1 预防心肌成纤维细胞激活和胶原生成。
Eur Heart J. 2012 Sep;33(18):2360-9. doi: 10.1093/eurheartj/ehr389. Epub 2011 Oct 25.
10
An essential role for resident fibroblasts in experimental lung fibrosis is defined by lineage-specific deletion of high-affinity type II transforming growth factor β receptor.研究表明，通过谱系特异性敲除高亲和力 II 型转化生长因子β受体，可明确确定驻留成纤维细胞在实验性肺纤维化中的重要作用。
Am J Respir Crit Care Med. 2011 Jan 15;183(2):249-61. doi: 10.1164/rccm.201002-0279OC. Epub 2010 Aug 13.

引用本文的文献

1
Wilms tumor 1 impairs apoptotic clearance of fibroblasts in distal fibrotic lung lesions.肾母细胞瘤1损害远端肺纤维化病变中纤维母细胞的凋亡清除。
J Clin Invest. 2025 Jun 10;135(15). doi: 10.1172/JCI188819. eCollection 2025 Aug 1.
2
Cryopreservation of Human Adult Ventricular Tissue for the Preparation of Viable Myocardial Slices.用于制备活性心肌切片的成人心室组织的冷冻保存
Curr Protoc. 2024 Dec;4(12):e70068. doi: 10.1002/cpz1.70068.

本文引用的文献

1
Temporal expression and spatial distribution of the proteoglycan versican during cardiac fibrosis development.心脏纤维化发展过程中蛋白聚糖多功能蛋白聚糖的时间表达和空间分布
Matrix Biol Plus. 2023 Nov 10;19-20:100135. doi: 10.1016/j.mbplus.2023.100135. eCollection 2023 Dec.
2
Cardiac fibroblasts and mechanosensation in heart development, health and disease.心脏成纤维细胞与心肌机械感知在心脏发育、健康和疾病中的作用。
Nat Rev Cardiol. 2023 May;20(5):309-324. doi: 10.1038/s41569-022-00799-2. Epub 2022 Nov 14.
3
Multicellular 3D Models for the Study of Cardiac Fibrosis.
用于心脏纤维化研究的多细胞 3D 模型。
Int J Mol Sci. 2022 Oct 1;23(19):11642. doi: 10.3390/ijms231911642.
4
Transforming growth factor-β in myocardial disease.转化生长因子-β 在心肌疾病中的作用。
Nat Rev Cardiol. 2022 Jul;19(7):435-455. doi: 10.1038/s41569-021-00646-w. Epub 2022 Jan 4.
5
Cardiomyocytes Cellular Phenotypes After Myocardial Infarction.心肌梗死后的心肌细胞表型
Front Cardiovasc Med. 2021 Nov 8;8:750510. doi: 10.3389/fcvm.2021.750510. eCollection 2021.
6
Guidelines for in vivo mouse models of myocardial infarction.心肌梗死体内小鼠模型的指南。
Am J Physiol Heart Circ Physiol. 2021 Dec 1;321(6):H1056-H1073. doi: 10.1152/ajpheart.00459.2021. Epub 2021 Oct 8.
7
Superimposed Tissue Formation in Human Aortic Valve Disease: Differences between Regurgitant and Stenotic Valves.人类主动脉瓣疾病中的叠加组织形成：反流性瓣膜与狭窄性瓣膜之间的差异
J Cardiovasc Dev Dis. 2021 Jul 8;8(7):79. doi: 10.3390/jcdd8070079.
8
Management of cardiac fibrosis is the largest unmet medical need in heart failure.心脏纤维化的管理是心力衰竭领域尚未满足的最大医疗需求。
Cardiovasc Res. 2022 Jan 29;118(2):e20-e22. doi: 10.1093/cvr/cvab228.
9
New calcification model for intact murine aortic valves.完整鼠主动脉瓣新钙化模型。
J Mol Cell Cardiol. 2021 Jul;156:95-104. doi: 10.1016/j.yjmcc.2021.03.003. Epub 2021 Mar 18.
10
Cardiac fibrosis.心肌纤维化。
Cardiovasc Res. 2021 May 25;117(6):1450-1488. doi: 10.1093/cvr/cvaa324.