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©2013 Baishideng Publishing Group Co.
World J Gastroenterol. May 21, 2013; 19(19): 2921-2934
Published online May 21, 2013. doi: 10.3748/wjg.v19.i19.2921
Published online May 21, 2013. doi: 10.3748/wjg.v19.i19.2921
Figure 7 Iron is involved in the heme oxygenase-1 cycle via the nuclear factor-E2-related factor 2/Keap1 pathway, and heme oxygenase-1 regulates portal pressure in liver cirrhosis.
Low hepcidin and heme oxygenase-1 (HO-1) over-expression could mediate iron accumulation, which accelerates oxidative stress, leading to cell injury, and it also increases HO-1 expression through the nuclear factor-E2-related factor 2 (Nrf2)/Keap1 pathway. Nrf2 protects cells against oxidative stress, but this effect is limited, and Nrf2 contributes to induction of HO-1 expression, which can produce iron. HO-1 can increase carbon monoxide (CO) production, and an unbalanced CO/nitric oxide system could play a role in portal pressure. ROS: Reactive oxygen species. ARE: Antioxidant response element.
- Citation: Wang QM, Du JL, Duan ZJ, Guo SB, Sun XY, Liu Z. Inhibiting heme oxygenase-1 attenuates rat liver fibrosis by removing iron accumulation. World J Gastroenterol 2013; 19(19): 2921-2934
- URL: https://www.wjgnet.com/1007-9327/full/v19/i19/2921.htm
- DOI: https://dx.doi.org/10.3748/wjg.v19.i19.2921