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慢性缺氧诱导肾细胞生长的机制。

Mechanisms of chronic hypoxia-induced renal cell growth.

作者信息

Sahai A, Mei C, Schrier R W, Tannen R L

机构信息

Division of Nephrology and Hypertension, Northwestern University Medical School, Chicago, Illinois 60611-3010, USA.

出版信息

Kidney Int. 1999 Oct;56(4):1277-81. doi: 10.1046/j.1523-1755.1999.00703.x.

DOI:10.1046/j.1523-1755.1999.00703.x
PMID:10504474
Abstract

Chronic local tissue hypoxia appears to play an important role in the initiation and progression of chronic renal disease. We examined the effect of local hypoxia on cultured renal tubular epithelial and mesangial cell proliferation, dedifferentiation, and extracellular matrix synthesis. The underlying signaling mechanisms whereby hypoxia induces renal cell growth were evaluated. The roles of protein kinase C, p38 mitogen-activated protein kinase, TGF-beta1, osteopontin, and nitric oxide were determined.

摘要

慢性局部组织缺氧似乎在慢性肾病的发生和发展中起重要作用。我们研究了局部缺氧对培养的肾小管上皮细胞和系膜细胞增殖、去分化及细胞外基质合成的影响。评估了缺氧诱导肾细胞生长的潜在信号传导机制。确定了蛋白激酶C、p38丝裂原活化蛋白激酶、转化生长因子-β1、骨桥蛋白和一氧化氮的作用。

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Mechanisms of chronic hypoxia-induced renal cell growth.慢性缺氧诱导肾细胞生长的机制。
Kidney Int. 1999 Oct;56(4):1277-81. doi: 10.1046/j.1523-1755.1999.00703.x.
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Osteopontin mediates hypoxia-induced proliferation of cultured mesangial cells: role of PKC and p38 MAPK.骨桥蛋白介导缺氧诱导的培养系膜细胞增殖:蛋白激酶C和p38丝裂原活化蛋白激酶的作用
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Hypoxia induces renal tubular epithelial cell apoptosis in chronic renal disease.缺氧在慢性肾脏疾病中诱导肾小管上皮细胞凋亡。
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