• 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

相似文献

1
Understanding cardiac extracellular matrix remodeling to develop biomarkers of myocardial infarction outcomes.了解心脏细胞外基质重构以开发心肌梗死结果的生物标志物。
Matrix Biol. 2019 Jan;75-76:43-57. doi: 10.1016/j.matbio.2017.12.001. Epub 2017 Dec 14.
2
A Novel Collagen Matricryptin Reduces Left Ventricular Dilation Post-Myocardial Infarction by Promoting Scar Formation and Angiogenesis.一种新型胶原蛋白基质金属蛋白酶抑制因子通过促进瘢痕形成和血管生成减少心肌梗死后左心室扩张。
J Am Coll Cardiol. 2015 Sep 22;66(12):1364-74. doi: 10.1016/j.jacc.2015.07.035.
3
Extracellular matrix remodeling following myocardial injury.心肌损伤后的细胞外基质重塑
Ann Med. 2003;35(5):316-26. doi: 10.1080/07853890310001285.
4
Reduced scar maturation and contractility lead to exaggerated left ventricular dilation after myocardial infarction in mice lacking AMPKα1.在缺乏AMPKα1的小鼠中,瘢痕成熟和收缩性降低导致心肌梗死后左心室扩张加剧。
J Mol Cell Cardiol. 2014 Sep;74:32-43. doi: 10.1016/j.yjmcc.2014.04.018. Epub 2014 May 5.
5
MMP induction and inhibition in myocardial infarction.心肌梗死中基质金属蛋白酶的诱导与抑制
Heart Fail Rev. 2004 Jan;9(1):7-19. doi: 10.1023/B:HREV.0000011390.44039.b7.
6
MMP-9 signaling in the left ventricle following myocardial infarction.心肌梗死后左心室中的 MMP-9 信号转导。
Am J Physiol Heart Circ Physiol. 2016 Jul 1;311(1):H190-8. doi: 10.1152/ajpheart.00243.2016. Epub 2016 May 20.
7
Matrix metalloproteinases as input and output signals for post-myocardial infarction remodeling.基质金属蛋白酶作为心肌梗死后重塑的输入和输出信号
J Mol Cell Cardiol. 2016 Feb;91:134-40. doi: 10.1016/j.yjmcc.2015.12.018. Epub 2015 Dec 23.
8
Myofibroblasts and the extracellular matrix network in post-myocardial infarction cardiac remodeling.心肌梗死后心脏重构中的肌成纤维细胞和细胞外基质网络。
Pflugers Arch. 2014 Jun;466(6):1113-27. doi: 10.1007/s00424-014-1463-9. Epub 2014 Feb 13.
9
Understanding the mechanisms that determine extracellular matrix remodeling in the infarcted myocardium.了解决定梗死心肌细胞外基质重塑的机制。
Biochem Soc Trans. 2019 Dec 20;47(6):1679-1687. doi: 10.1042/BST20190113.
10
Mapping macrophage polarization over the myocardial infarction time continuum.描绘心肌梗死时间连续体上的巨噬细胞极化。
Basic Res Cardiol. 2018 Jun 4;113(4):26. doi: 10.1007/s00395-018-0686-x.

引用本文的文献

1
Matrix Metalloproteinases 7 and 10 Are Prognostic Biomarkers for Systemic Cardiovascular Risk in Individuals with Peripheral Artery Disease.基质金属蛋白酶7和10是外周动脉疾病患者全身心血管风险的预后生物标志物。
Biomolecules. 2025 Jun 11;15(6):853. doi: 10.3390/biom15060853.
2
Sex differences in the chronic autoimmune response to myocardial infarction.心肌梗死慢性自身免疫反应中的性别差异。
Clin Sci (Lond). 2025 Jun 17;139(12):627-48. doi: 10.1042/CS20243091.
3
Regulatory T cells: a promising new therapeutic target in ventricular remodeling after myocardial infarction.调节性T细胞:心肌梗死后心室重构中一个有前景的新治疗靶点。
Front Immunol. 2025 Apr 7;16:1514335. doi: 10.3389/fimmu.2025.1514335. eCollection 2025.
4
Harnessing synergistic effects of MMP-2 Inhibition and bFGF to simultaneously preserve and vascularize cardiac extracellular matrix after myocardial infarction.利用基质金属蛋白酶-2抑制和碱性成纤维细胞生长因子的协同作用,在心肌梗死后同时保留心脏细胞外基质并使其血管化。
Acta Biomater. 2025 Jan 1;191:189-204. doi: 10.1016/j.actbio.2024.10.050. Epub 2024 Nov 12.
5
Comparative Analysis of Plasma Protein Dynamics in Women with ST-Elevation Myocardial Infarction and Takotsubo Syndrome.女性 ST 段抬高型心肌梗死与心尖球形综合征患者血浆蛋白动力学的对比分析。
Cells. 2024 Oct 24;13(21):1764. doi: 10.3390/cells13211764.
6
Persistent Ferroptosis Modulates Cardiac Remodeling and M2 Macrophage Polarization, Which Can be Mitigated by Astaxanthin During Myocardial Infarction Recovery.持续性铁死亡调节心脏重塑和M2巨噬细胞极化,在心肌梗死恢复过程中虾青素可减轻这种情况。
Cardiovasc Toxicol. 2025 Jan;25(1):58-73. doi: 10.1007/s12012-024-09942-6. Epub 2024 Nov 4.
7
Screening for Heart Failure: Biomarkers to Detect Heightened Risk in the General Population.心力衰竭筛查:在普通人群中检测风险升高的生物标志物。
Curr Heart Fail Rep. 2024 Dec;21(6):591-603. doi: 10.1007/s11897-024-00686-6. Epub 2024 Sep 17.
8
Mechanisms of assembly and remodelling of the extracellular matrix.细胞外基质的组装和重塑机制。
Nat Rev Mol Cell Biol. 2024 Nov;25(11):865-885. doi: 10.1038/s41580-024-00767-3. Epub 2024 Sep 2.
9
Egr1 regulates regenerative senescence and cardiac repair.Egr1 调节再生性衰老和心脏修复。
Nat Cardiovasc Res. 2024 Aug;3(8):915-932. doi: 10.1038/s44161-024-00493-1. Epub 2024 Jun 14.
10
Microtubules Sequester Acetylated YAP in the Cytoplasm and Inhibit Heart Regeneration.微管将乙酰化的YAP隔离于细胞质中并抑制心脏再生。
Circulation. 2025 Jan 7;151(1):59-75. doi: 10.1161/CIRCULATIONAHA.123.067646. Epub 2024 Aug 26.

本文引用的文献

1
Methylglyoxal-derived advanced glycation end products contribute to negative cardiac remodeling and dysfunction post-myocardial infarction.甲基乙二醛衍生的晚期糖基化终产物导致心肌梗死后心脏重构和功能障碍恶化。
Basic Res Cardiol. 2017 Sep 1;112(5):57. doi: 10.1007/s00395-017-0646-x.
2
Autoantibodies against basement membrane collagen type IV are associated with myocardial infarction.抗IV型基底膜胶原蛋白自身抗体与心肌梗死有关。
Int J Cardiol Heart Vasc. 2014 Dec 30;6:42-47. doi: 10.1016/j.ijcha.2014.12.003. eCollection 2015 Mar 1.
3
Detrimental role of lysyl oxidase in cardiac remodeling.赖氨酰氧化酶在心脏重构中的有害作用。
J Mol Cell Cardiol. 2017 Aug;109:17-26. doi: 10.1016/j.yjmcc.2017.06.013. Epub 2017 Jun 29.
4
Clinical Implications of Compounds Designed to Inhibit ECM-Modifying Metalloproteinases.旨在抑制细胞外基质修饰金属蛋白酶的化合物的临床意义。
Proteomics. 2017 Dec;17(23-24). doi: 10.1002/pmic.201600389. Epub 2017 Sep 15.
5
The extracellular matrix in myocardial injury, repair, and remodeling.心肌损伤、修复与重塑中的细胞外基质
J Clin Invest. 2017 May 1;127(5):1600-1612. doi: 10.1172/JCI87491.
6
IL-10 improves cardiac remodeling after myocardial infarction by stimulating M2 macrophage polarization and fibroblast activation.白细胞介素-10通过刺激M2巨噬细胞极化和成纤维细胞活化来改善心肌梗死后的心脏重塑。
Basic Res Cardiol. 2017 May;112(3):33. doi: 10.1007/s00395-017-0622-5. Epub 2017 Apr 24.
7
Non-invasive quantification of collagen turnover in renal transplant recipients.肾移植受者胶原蛋白更新的非侵入性定量分析
PLoS One. 2017 Apr 21;12(4):e0175898. doi: 10.1371/journal.pone.0175898. eCollection 2017.
8
Extracellular matrix markers and risk of myocardial infarction: The HUNT Study in Norway.细胞外基质标志物与心肌梗死风险:挪威 HUNT 研究。
Eur J Prev Cardiol. 2017 Jul;24(11):1161-1167. doi: 10.1177/2047487317703826. Epub 2017 Apr 21.
9
Matrix Metalloproteinases in Myocardial Infarction and Heart Failure.心肌梗死与心力衰竭中的基质金属蛋白酶
Prog Mol Biol Transl Sci. 2017;147:75-100. doi: 10.1016/bs.pmbts.2017.02.001. Epub 2017 Mar 18.
10
Serum endotrophin, a type VI collagen cleavage product, is associated with increased mortality in chronic kidney disease.血清内营养蛋白,一种VI型胶原蛋白裂解产物,与慢性肾脏病死亡率增加相关。
PLoS One. 2017 Apr 12;12(4):e0175200. doi: 10.1371/journal.pone.0175200. eCollection 2017.

了解心脏细胞外基质重构以开发心肌梗死结果的生物标志物。

Understanding cardiac extracellular matrix remodeling to develop biomarkers of myocardial infarction outcomes.

机构信息

Fibrosis Biology and Biomarkers, Nordic Bioscience, Herlev, Denmark; Disease Systems Immunology, Technical University of Denmark, Kgs. Lyngby, Denmark.

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

出版信息

Matrix Biol. 2019 Jan;75-76:43-57. doi: 10.1016/j.matbio.2017.12.001. Epub 2017 Dec 14.

DOI:10.1016/j.matbio.2017.12.001
PMID:29247693
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6002886/
Abstract

Cardiovascular Disease (CVD) is the most common cause of death in industrialized countries, and myocardial infarction (MI) is a major CVD with significant morbidity and mortality. Following MI, the left ventricle (LV) undergoes a wound healing response to ischemia that results in extracellular matrix (ECM) scar formation to replace necrotic myocytes. While ECM accumulation following MI is termed cardiac fibrosis, this is a generic term that does not differentiate between ECM accumulation that occurs in the infarct region to form a scar that is structurally necessary to preserve left ventricle (LV) wall integrity and ECM accumulation that increases LV wall stiffness to exacerbate dilation and stimulate the progression to heart failure. This review focuses on post-MI LV ECM remodeling, targeting the discussion on ECM biomarkers that could be useful for predicting MI outcomes.

摘要

心血管疾病(CVD)是工业化国家中最常见的死亡原因,心肌梗死(MI)是一种主要的 CVD,具有显著的发病率和死亡率。MI 后,左心室(LV)对缺血发生伤口愈合反应,导致细胞外基质(ECM)瘢痕形成以替代坏死的心肌细胞。虽然 MI 后 ECM 的积累被称为心脏纤维化,但这是一个通用术语,并不能区分在梗死区域发生的 ECM 积累以形成对维持左心室(LV)壁完整性结构上必需的瘢痕,以及增加 LV 壁僵硬以加剧扩张并刺激进展为心力衰竭的 ECM 积累。这篇综述重点介绍了 MI 后 LV ECM 重塑,针对 ECM 生物标志物的讨论可能对预测 MI 结局有用。