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缺血性和中毒性肾小管细胞损伤的生物学机制:一氧化氮及炎症反应的作用

Biology of ischemic and toxic renal tubular cell injury: role of nitric oxide and the inflammatory response.

作者信息

Lieberthal W

机构信息

Evans Department of Clinical Research, Boston Medical Center, Boston University Medical School, Massachusetts, USA.

出版信息

Curr Opin Nephrol Hypertens. 1998 May;7(3):289-95. doi: 10.1097/00041552-199805000-00009.

DOI:10.1097/00041552-199805000-00009
PMID:9617560
Abstract

Acute ischemic or toxic injury to the kidney induces alterations in the expression of many genes. Some of these molecular responses have been termed 'maladaptive' because they exacerbate the tubular damage induced by the initiating insult. Some maladaptive responses include alterations in the activity of nitric oxide synthases and expression of cytokines and adhesion molecules that mediate an inflammatory response. This review focuses on the role of nitric oxide and inflammation in influencing the course of acute renal failure due to ischemic and toxic tubular injury.

摘要

肾脏的急性缺血性或中毒性损伤会导致许多基因表达发生改变。其中一些分子反应被称为“适应性不良”,因为它们会加剧初始损伤所引发的肾小管损伤。一些适应性不良反应包括一氧化氮合酶活性的改变以及介导炎症反应的细胞因子和黏附分子的表达。本综述重点关注一氧化氮和炎症在影响缺血性和中毒性肾小管损伤所致急性肾衰竭病程中的作用。

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