Cellular mechanisms of cardiac hypertrophy.
作者信息
Glennon P E, Sugden P H, Poole-Wilson P A
机构信息
Department of Cardiac Medicine, National Heart and Lung Institute, London.
出版信息
Br Heart J. 1995 Jun;73(6):496-9. doi: 10.1136/hrt.73.6.496.
Abstract
摘要
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Cellular mechanisms of cardiac hypertrophy.心脏肥大的细胞机制
Br Heart J. 1995 Jun;73(6):496-9. doi: 10.1136/hrt.73.6.496.
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本文引用的文献
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Hypertrophy or hyperplasia in cardiac muscle. Post-mortem human morphometric study.心肌肥大或增生。人体尸检形态计量学研究。
Eur Heart J. 1993 Jan;14(1):40-7. doi: 10.1093/eurheartj/14.1.40.
2
HRas-dependent pathways can activate morphological and genetic markers of cardiac muscle cell hypertrophy.依赖HRas的信号通路可激活心肌细胞肥大的形态学和遗传学标志物。
J Biol Chem. 1993 Jan 25;268(3):2244-9.
3
A dominant-negative mutant of raf blocks mitogen-activated protein kinase activation by growth factors and oncogenic p21ras.raf的显性负性突变体可阻断生长因子和致癌性p21ras介导的丝裂原活化蛋白激酶激活。
J Biol Chem. 1993 Sep 25;268(27):20232-6.
4
5
Mechanical stretch rapidly activates multiple signal transduction pathways in cardiac myocytes: potential involvement of an autocrine/paracrine mechanism.机械牵张可迅速激活心肌细胞中的多种信号转导通路：自分泌/旁分泌机制的潜在参与。
EMBO J. 1993 Apr;12(4):1681-92. doi: 10.1002/j.1460-2075.1993.tb05813.x.
6
Endothelin-1, phorbol esters and phenylephrine stimulate MAP kinase activities in ventricular cardiomyocytes.内皮素-1、佛波酯和去氧肾上腺素可刺激心室心肌细胞中的丝裂原活化蛋白激酶活性。
FEBS Lett. 1993 Feb 15;317(3):271-5. doi: 10.1016/0014-5793(93)81291-7.
7
Signal transduction pathways of angiotensin II--induced c-fos gene expression in cardiac myocytes in vitro. Roles of phospholipid-derived second messengers.血管紧张素II诱导体外培养心肌细胞中c-fos基因表达的信号转导途径。磷脂衍生的第二信使的作用。
Circ Res. 1993 Sep;73(3):424-38. doi: 10.1161/01.res.73.3.424.
8
Molecular characterization of angiotensin II--induced hypertrophy of cardiac myocytes and hyperplasia of cardiac fibroblasts. Critical role of the AT1 receptor subtype.血管紧张素II诱导心肌细胞肥大和心脏成纤维细胞增生的分子特征。AT1受体亚型的关键作用。
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Defects in heart and lung development in compound heterozygotes for two different targeted mutations at the N-myc locus.N-myc基因座上两个不同靶向突变的复合杂合子中心脏和肺部发育的缺陷。
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