期刊
CURRENT PHARMACEUTICAL BIOTECHNOLOGY
卷 13, 期 6, 页码 819-826出版社
BENTHAM SCIENCE PUBL LTD
DOI: 10.2174/138920112800399284
关键词
Heme oxygenase; renal failure; blood pressure; bilirubin; acute renal injury
资金
- University of Mississippi Medical Center
- National Heart, Lung, and Blood Institute [HL088421, HL088421-S1, PO1HL-5197]
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.
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