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The extracellular matrix in normal and diseased myocardium.

作者信息

Hein S, Schaper J

机构信息

Kerckhoff Clinic, Department of Cardiac Surgery, Bad Nauheim, Germany.

出版信息

J Nucl Cardiol. 2001 Mar-Apr;8(2):188-96. doi: 10.1067/mnc.2001.113331.

DOI:10.1067/mnc.2001.113331
PMID:11295697
Abstract
摘要

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The extracellular matrix in normal and diseased myocardium.正常和患病心肌中的细胞外基质。
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本文引用的文献

1
Fibronectin accumulation within cardiac myocytes in rats with elevated plasma angiotensin II.
Cardiovasc Pathol. 1995 Jan-Mar;4(1):57-67. doi: 10.1016/1054-8807(94)00042-p.
2
Disruption of the myocardial extracellular matrix leads to cardiac dysfunction.心肌细胞外基质的破坏会导致心脏功能障碍。
J Clin Invest. 2000 Oct;106(7):857-66. doi: 10.1172/JCI8040.
3
Lisinopril-mediated regression of myocardial fibrosis in patients with hypertensive heart disease.赖诺普利介导高血压性心脏病患者心肌纤维化的消退
个性化心脏计算模型：从临床数据到梗死相关室性心动过速的模拟
Front Physiol. 2019 May 15;10:580. doi: 10.3389/fphys.2019.00580. eCollection 2019.
4
Collagen biomaterial for the treatment of myocardial infarction: an update on cardiac tissue engineering and myocardial regeneration.胶原生物材料治疗心肌梗死：心脏组织工程和心肌再生的最新进展。
Drug Deliv Transl Res. 2019 Oct;9(5):920-934. doi: 10.1007/s13346-019-00627-0.
5
Quantitative temporal analysis of protein dynamics in cardiac remodeling.心肌重构中蛋白质动力学的定量时间分析。
J Mol Cell Cardiol. 2018 Aug;121:163-172. doi: 10.1016/j.yjmcc.2018.07.126. Epub 2018 Jul 19.
6
Evaluation of serum prolidase activity in patients with slow coronary flow.冠状动脉血流缓慢患者血清脯氨酰二肽氨基肽酶活性的评估。
Postepy Kardiol Interwencyjnej. 2015;11(3):206-11. doi: 10.5114/pwki.2015.54015. Epub 2015 Sep 28.
7
Aging and the cardiac collagen matrix: Novel mediators of fibrotic remodelling.衰老与心脏胶原基质：纤维化重塑的新型介质
J Mol Cell Cardiol. 2016 Apr;93:175-85. doi: 10.1016/j.yjmcc.2015.11.005. Epub 2015 Nov 11.
8
Animal Models and "Omics" Technologies for Identification of Novel Biomarkers and Drug Targets to Prevent Heart Failure.用于识别预防心力衰竭的新型生物标志物和药物靶点的动物模型与“组学”技术
Biomed Res Int. 2015;2015:212910. doi: 10.1155/2015/212910. Epub 2015 Jul 7.
9
Strategies for the chemical and biological functionalization of scaffolds for cardiac tissue engineering: a review.用于心脏组织工程的支架的化学和生物功能化策略：综述
J R Soc Interface. 2015 Jul 6;12(108):20150254. doi: 10.1098/rsif.2015.0254.
10
Stable, covalent attachment of laminin to microposts improves the contractility of mouse neonatal cardiomyocytes.层粘连蛋白与微柱的稳定共价连接可改善小鼠新生心肌细胞的收缩性。
ACS Appl Mater Interfaces. 2014 Sep 10;6(17):15516-26. doi: 10.1021/am5042324. Epub 2014 Aug 26.
Circulation. 2000 Sep 19;102(12):1388-93. doi: 10.1161/01.cir.102.12.1388.
4
Outside-in signalling of fibronectin stimulates cardiomyocyte hypertrophy in cultured neonatal rat ventricular myocytes.纤连蛋白的外向信号传导刺激培养的新生大鼠心室肌细胞肥大。
J Mol Cell Cardiol. 2000 May;32(5):765-76. doi: 10.1006/jmcc.2000.1119.
5
Expression of laminin alpha2 chain during normal and pathological growth of myocardium in rat and human.层粘连蛋白α2链在大鼠和人类心肌正常及病理生长过程中的表达
Cardiovasc Res. 2000 May;46(2):346-55. doi: 10.1016/s0008-6363(00)00034-1.
6
Myocardial matrix degradation and metalloproteinase activation in the failing heart: a potential therapeutic target.衰竭心脏中的心肌基质降解与金属蛋白酶激活：一个潜在的治疗靶点。
Cardiovasc Res. 2000 May;46(2):225-38. doi: 10.1016/s0008-6363(99)00431-9.
7
Serum carboxy-terminal propeptide of procollagen type I is a marker of myocardial fibrosis in hypertensive heart disease.血清I型前胶原羧基末端前肽是高血压性心脏病心肌纤维化的一个标志物。
Circulation. 2000 Apr 11;101(14):1729-35. doi: 10.1161/01.cir.101.14.1729.
8
Diastolic heart failure.舒张性心力衰竭
Cardiovasc Res. 2000 Mar;45(4):813-25. doi: 10.1016/s0008-6363(99)00399-5.
9
Cardiac remodeling--concepts and clinical implications: a consensus paper from an international forum on cardiac remodeling. Behalf of an International Forum on Cardiac Remodeling.心脏重塑——概念与临床意义：心脏重塑国际论坛共识文件。代表心脏重塑国际论坛。
J Am Coll Cardiol. 2000 Mar 1;35(3):569-82. doi: 10.1016/s0735-1097(99)00630-0.
10
Morphology and significance of the left ventricular collagen network in young patients with hypertrophic cardiomyopathy and sudden cardiac death.肥厚型心肌病合并心源性猝死年轻患者左心室胶原网络的形态学及意义
J Am Coll Cardiol. 2000 Jan;35(1):36-44. doi: 10.1016/s0735-1097(99)00492-1.