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[分子生物学视角下肾小球硬化症中的肾小球细胞外基质]

[Glomerular extracellular matrix in glomerulosclerosis by molecular biology].

作者信息

Makino H

机构信息

Third Department of Internal Medicine, Okayama University Medical School.

出版信息

Nihon Rinsho. 1992 Dec;50(12):3038-45.

PMID:1491457
Abstract

Many renal diseases progress to end-stage renal failure with glomerulosclerosis, irrespective of the cause of the disease. Glomerulosclerosis is characterized by an accumulation of extracellular matrices (ECM) due to increased synthesis of the ECM and/or decreased degradation of the ECM. Sclerotic lesions represent an accumulation of normal constituents of the ECM, including type IV collagen, laminin, proteoglycans, as well as, abnormal constituents such as type I and III collagens. The cDNAs for various ECM constituents have been obtained and it has become possible to study the status of their synthesis, in the transcriptional level, in various glomerular diseases. Studies suggest that hemodynamic factors and growth factors, such as, TGF-beta and PDGF are responsible for the development of glomerulosclerosis. Inappropriate expression of intrinsic mesangial cell metalloproteinases and tissue inhibitors of metalloproteinases also lead to glomerulosclerosis.

摘要

许多肾脏疾病都会发展为伴有肾小球硬化的终末期肾衰竭,无论其病因如何。肾小球硬化的特征是细胞外基质(ECM)的积累,这是由于ECM合成增加和/或ECM降解减少所致。硬化性病变代表了ECM正常成分的积累,包括IV型胶原、层粘连蛋白、蛋白聚糖,以及I型和III型胶原等异常成分。已经获得了各种ECM成分的cDNA,并且在转录水平上研究它们在各种肾小球疾病中的合成状态成为可能。研究表明,血流动力学因素和生长因子,如转化生长因子-β(TGF-β)和血小板衍生生长因子(PDGF),是肾小球硬化发展的原因。固有系膜细胞金属蛋白酶和金属蛋白酶组织抑制剂的不适当表达也会导致肾小球硬化。

相似文献

1
[Glomerular extracellular matrix in glomerulosclerosis by molecular biology].[分子生物学视角下肾小球硬化症中的肾小球细胞外基质]
Nihon Rinsho. 1992 Dec;50(12):3038-45.
2
Differential expression of glomerular extracellular matrix and growth factor mRNA in rapid and slowly progressive glomerulosclerosis: studies in mice transgenic for native or mutated growth hormone.快速和缓慢进展性肾小球硬化中肾小球细胞外基质和生长因子mRNA的差异表达:对天然或突变生长激素转基因小鼠的研究
Lab Invest. 1997 Apr;76(4):467-76.
3
A histologic study of the extracellular matrix during the development of glomerulosclerosis in murine chronic graft-versus-host disease.小鼠慢性移植物抗宿主病肾小球硬化症发展过程中细胞外基质的组织学研究
Am J Pathol. 1992 May;140(5):1147-56.
4
[Role of TGF-beta in glomerular diseases].[转化生长因子-β在肾小球疾病中的作用]
Nihon Rinsho. 1992 Dec;50(12):3032-7.
5
Role of the extracellular matrix in the development of glomerulosclerosis in experimental chronic serum sickness.细胞外基质在实验性慢性血清病肾小球硬化症发展中的作用
Exp Nephrol. 1995 Nov-Dec;3(6):338-47.
6
Glomerulosclerosis induced by in vivo transfection of transforming growth factor-beta or platelet-derived growth factor gene into the rat kidney.通过将转化生长因子-β或血小板衍生生长因子基因体内转染至大鼠肾脏所诱导的肾小球硬化。
J Clin Invest. 1993 Dec;92(6):2597-601. doi: 10.1172/JCI116874.
7
Glomerular cells, extracellular matrix accumulation, and the development of glomerulosclerosis in the remnant kidney model.肾小球细胞、细胞外基质积聚与残余肾模型中肾小球硬化的发展
Lab Invest. 1992 Apr;66(4):485-97.
8
Enhanced proliferation, apoptosis, and matrix accumulation by mesangial cells derived from HIV-1 transgenic mice.源自HIV-1转基因小鼠的系膜细胞增殖、凋亡及基质积累增强。
J Investig Med. 1998 Aug;46(6):297-302.
9
The mesangial matrix in the normal and sclerotic glomerulus.正常及硬化肾小球中的系膜基质。
Kidney Int Suppl. 1994 Feb;45:S73-7.
10
Time course study of the extracellular matrix in puromycin-aminonucleoside-induced glomerulosclerosis.嘌呤霉素氨基核苷诱导的肾小球硬化症细胞外基质的时间进程研究
Nihon Jinzo Gakkai Shi. 1994 Apr;36(4):307-16.

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