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2
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本文引用的文献

1
Reinforcing feedback loop of renal cyclic guanosine 3' 5' -monophosphate and interstitial hydrostatic pressure in pressure-natriuresis.压力性利钠中肾环磷酸鸟苷与间质静水压的增强反馈回路
Hypertension. 2009 Dec;54(6):1278-83. doi: 10.1161/HYPERTENSIONAHA.109.131995. Epub 2009 Oct 19.
2
Dual pathways of carbon monoxide-mediated vasoregulation: modulation by redox mechanisms.一氧化碳介导的血管调节的双重途径:氧化还原机制的调节
Circ Res. 2009 Oct 9;105(8):775-83. doi: 10.1161/CIRCRESAHA.109.197434. Epub 2009 Sep 10.
3
Activation of PPAR-gamma by carbon monoxide from CORM-2 leads to the inhibition of iNOS but not COX-2 expression in LPS-stimulated macrophages.一氧化碳供体 CORM-2 激活 PPAR-γ可抑制 LPS 刺激的巨噬细胞中 iNOS 但不 COX-2 的表达。
Inflammation. 2009 Dec;32(6):364-71. doi: 10.1007/s10753-009-9144-0.
4
Low-dose carbon monoxide inhibits progressive chronic allograft nephropathy and restores renal allograft function.低剂量一氧化碳可抑制进行性慢性移植肾肾病并恢复移植肾功能。
Am J Physiol Renal Physiol. 2009 Jul;297(1):F19-26. doi: 10.1152/ajprenal.90728.2008. Epub 2009 Apr 15.
5
Hemin therapy attenuates kidney injury in deoxycorticosterone acetate-salt hypertensive rats.血红素疗法可减轻醋酸脱氧皮质酮-盐高血压大鼠的肾损伤。
Am J Physiol Renal Physiol. 2009 Mar;296(3):F521-34. doi: 10.1152/ajprenal.00510.2007. Epub 2008 Dec 30.
6
Heme oxygenase metabolites inhibit tubuloglomerular feedback (TGF).血红素加氧酶代谢产物抑制肾小管-肾小球反馈(TGF)。
Am J Physiol Renal Physiol. 2008 Oct;295(4):F1207-12. doi: 10.1152/ajprenal.90243.2008. Epub 2008 Aug 20.
7
Heme oxygenase attenuates angiotensin II-mediated superoxide production in cultured mouse thick ascending loop of Henle cells.血红素加氧酶可减弱血管紧张素 II 介导的培养小鼠髓袢升支粗段细胞中超氧化物的产生。
Am J Physiol Renal Physiol. 2008 Oct;295(4):F1158-65. doi: 10.1152/ajprenal.00057.2008. Epub 2008 Aug 13.
8
Kidney-specific induction of heme oxygenase-1 prevents angiotensin II hypertension.肾脏特异性诱导血红素加氧酶-1可预防血管紧张素II性高血压。
Hypertension. 2008 Oct;52(4):660-5. doi: 10.1161/HYPERTENSIONAHA.108.114884. Epub 2008 Aug 11.
9
cGMP decreases surface NKCC2 levels in the thick ascending limb: role of phosphodiesterase 2 (PDE2).环磷酸鸟苷(cGMP)降低髓袢升支粗段表面的钠-钾-2氯协同转运蛋白2(NKCC2)水平:磷酸二酯酶2(PDE2)的作用
Am J Physiol Renal Physiol. 2008 Oct;295(4):F877-87. doi: 10.1152/ajprenal.00449.2007. Epub 2008 Aug 6.
10
Heme oxygenase induction attenuates afferent arteriolar autoregulatory responses.血红素加氧酶的诱导减弱了入球小动脉的自身调节反应。
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一氧化碳在肾功能中的作用:少量一氧化碳对肾脏有益吗?

Role of carbon monoxide in kidney function: is a little carbon monoxide good for the kidney?

机构信息

Department of Physiology & Biophysics, Center for Excellence in Cardiovascular-Renal Research, University of Mississippi Medical Center, Jackson, MS 39216, USA.

出版信息

Curr Pharm Biotechnol. 2012 May;13(6):819-26. doi: 10.2174/138920112800399284.

DOI:10.2174/138920112800399284
PMID:22201605
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3354025/
Abstract

Carbon monoxide (CO) is an endogenously produced gas resulting from the degradation of heme by heme oxygense or from fatty acid oxidation. Heme oxygenase (HO) enzymes are constitutively expressed in the kidney (HO-2) and HO-1 is induced in the kidney in response to several physiological and pathological stimuli. While the beneficial actions of HO in the kidney have been recognized for some time, the important role of CO in mediating these effects has not been fully examined. Recent studies using CO inhalation therapy and carbon monoxide releasing molecules (CORMs) have demonstrated that increases in CO alone can be beneficial to the kidney in several forms of acute renal injury by limiting oxidative injury, decreasing cell apoptosis, and promoting cell survival pathways. Renal CO is also emerging as a major regulator of renal vascular and tubular function acting to protect the renal vasculature against excessive vasoconstriction and to promote natriuresis by limiting sodium reabsorption in tubule cells. Within this review, recent studies on the physiological actions of CO in the kidney will be explored as well as the potential therapeutic avenues that are being developed targeting CO in the kidney which may be beneficial in diseases such as acute renal failure and hypertension.

摘要

一氧化碳(CO)是一种内源性气体,由血红素氧合酶或脂肪酸氧化作用导致血红素降解而产生。血红素氧合酶(HO)在肾脏中持续表达(HO-2),HO-1 在受到多种生理和病理刺激时在肾脏中被诱导。虽然 HO 在肾脏中的有益作用已经被认识了一段时间,但 CO 在介导这些作用中的重要作用尚未得到充分研究。最近使用 CO 吸入治疗和一氧化碳释放分子(CORMs)的研究表明,单独增加 CO 就可以通过限制氧化损伤、减少细胞凋亡和促进细胞存活途径,对几种急性肾损伤形式的肾脏有益。肾脏 CO 也正在成为肾脏血管和管状功能的主要调节剂,通过防止肾脏血管过度收缩和通过限制肾小管细胞中钠的重吸收来促进排钠,从而保护肾脏血管。在这篇综述中,将探讨 CO 在肾脏中的生理作用的最新研究,以及针对肾脏中 CO 的潜在治疗途径,这可能对急性肾衰竭和高血压等疾病有益。