• 主题
高级搜索  >
历史搜索 清空历史
首页> 外文期刊>American Journal of Physiology >The story so far: Molecular regulation of the heme oxygenase-1 gene in renal injury.
【24h】

The story so far: Molecular regulation of the heme oxygenase-1 gene in renal injury.

机译：迄今为止的故事：肾损伤中血红素加氧酶-1基因的分子调控。

获取原文
获取原文并翻译 | 示例
           
页面导航
  • 摘要
  • 著录项
  • 相似文献
  • 相关主题

摘要

Heme oxygenases (HOs) catalyze the rate-limiting step in heme degradation, resulting in the formation of iron, carbon monoxide, and biliverdin, the latter of which is subsequently converted to bilirubin by biliverdin reductase. Recent attention has focused on the biological effects of product(s) of this enzymatic reaction, which have important antioxidant, anti-inflammatory, and cytoprotective functions. Two major isoforms of the HO enzyme have been described: an inducible isoform, HO-1, and a constitutively expressed isoform, HO-2. A third isoform, HO-3, closely related to HO-2, has also been described. Several stimuli implicated in the pathogenesis of renal injury, such as heme, nitric oxide, growth factors, angiotensin II, cytokines, and nephrotoxins, induce HO-1. Induction of HO-1 occurs as an adaptive and beneficial response to these stimuli, as demonstrated by studies in renal and non-renal disease states. This review will focus on the molecular regulation of the HO-1 gene in renal injury and will highlight the interspecies differences, predominantly between the rodent and human HO-1 genes.
机译：血红素加氧酶（HOs）催化血红素降解中的限速步骤，导致形成铁，一氧化碳和biliverdin，后者随后通过biliverdin还原酶转化为胆红素。最近的关注集中在这种酶促反应产物的生物学效应上，其具有重要的抗氧化剂，抗炎和细胞保护功能。已经描述了HO酶的两个主要同工型：可诱导同工型HO-1和组成型表达的同工型HO-2。还描述了与HO-2密切相关的第三同工型HO-3。与肾损伤的发病机理有关的几种刺激物，如血红素，一氧化氮，生长因子，血管紧张素II，细胞因子和肾毒素，可诱导HO-1。如对肾脏和非肾脏疾病状态的研究所证实的，HO-1的诱导是对这些刺激的适应性和有益反应。这项审查将侧重于肾脏损伤中HO-1基因的分子调控，并将突出种间差异，主要是啮齿动物和人HO-1基因之间的差异。

著录项

相似文献

  • 外文文献
  • 中文文献
  • 专利
获取原文

客服邮箱：kefu@zhangqiaokeyan.com

京公网安备：11010802029741号 ICP备案号：京ICP备15016152号-6 六维联合信息科技 (北京) 有限公司©版权所有

  • 客服微信

  • 服务号