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急性损伤后肾脏修复与存活的机制。

Mechanisms of renal repair and survival following acute injury.

作者信息

Safirstein R, DiMari J, Megyesi J, Price P

机构信息

University of Texas Medical Branch at Galveston, Department of Internal Medicine, 77555-0562, USA.

出版信息

Semin Nephrol. 1998 Sep;18(5):519-22.

PMID:9754604
Abstract

The reaction of the renal epithelium to injury is heterogenous. Some cells die, others survive apparently intact, while others commit to repair. The determinants of these responses appear to depend on signal transduction pathways and molecular responses that is segment specific and interactive. The kidney, as do cells in culture exposed to various noxious stimuli, react in a typical manner referred to as the stress response. The response is comprised of kinases and their molecular targets as well as cell cycle-specific factors that determine whether a cell survives the injury or not. We propose that this response can be modified by survival factors which upregulate those aspects of the response that are cytoprotective and which downregulate those that are cytoreductive. Preliminary data will be presented to demonstrate the feasibility of this approach.

摘要

肾上皮细胞对损伤的反应是异质性的。一些细胞死亡,另一些细胞看似完好地存活下来,还有一些细胞则致力于修复。这些反应的决定因素似乎取决于信号转导途径和分子反应,这些反应具有节段特异性且相互作用。肾脏与暴露于各种有害刺激的培养细胞一样,以一种称为应激反应的典型方式做出反应。这种反应由激酶及其分子靶点以及决定细胞能否在损伤中存活的细胞周期特异性因子组成。我们提出,这种反应可以被存活因子所改变,存活因子会上调反应中具有细胞保护作用的方面,而下调具有细胞还原作用的方面。将展示初步数据以证明这种方法的可行性。

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Mechanisms of renal repair and survival following acute injury.急性损伤后肾脏修复与存活的机制。
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2
Renal stress response and acute renal failure.肾应激反应与急性肾衰竭。
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Growth factors and acute renal failure.生长因子与急性肾衰竭
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D-Serine exposure resulted in gene expression changes indicative of activation of fibrogenic pathways and down-regulation of energy metabolism and oxidative stress response.D-丝氨酸暴露导致基因表达变化,提示促纤维化途径激活以及能量代谢和氧化应激反应下调。
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Extracellular signal-regulated kinase mediates renal regeneration in rats with myoglobinuric acute renal injury.细胞外信号调节激酶介导肌红蛋白尿性急性肾损伤大鼠的肾脏再生。
Biochem Biophys Res Commun. 1999 Jan 8;254(1):88-92. doi: 10.1006/bbrc.1998.9902.

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