期刊
ARCHIVES OF BIOCHEMISTRY AND BIOPHYSICS
卷 564, 期 -, 页码 83-88出版社
ELSEVIER SCIENCE INC
DOI: 10.1016/j.abb.2014.09.005
关键词
Heme oxygenase; Macrophage; Polarization; Inflammation
资金
- Japan Society for the Promotion of Science [25460958, 25460959, 25750050]
- Japan Science and Technology Agency
- Grants-in-Aid for Scientific Research [25460959, 25460958, 25750050] Funding Source: KAKEN
Heme oxygenase-1 (HO-1) catalyzes the first and rate-limiting enzymatic step of heme degradation and produces carbon monoxide, free iron, and biliverdin. HO-1, a stress-inducible protein, is induced by various oxidative and inflammatory signals. Consequently, HO-1 expression has been regarded as an adaptive cellular response against inflammatory response and oxidative injury. Although several transcriptional factors and signaling cascades are involved in HO-1 regulation, the two main pathways of Nrf2/Bach1 system and IL-10/HO-1 axis exist in monocyte/macrophage. Macrophages are broadly divisible into two groups: pro-inflammatory M1 macrophages and anti-inflammatory M2 macrophages. More recently, several novel macrophage subsets have been identified including Mhem. Mox, and M4 macrophages. Of these, M2 macrophages, Mhem, and Mox are HO-1 highly expressing macrophages. HO-1 has been recognized as having major immunomodulatory and anti-inflammatory properties, which have been demonstrated in HO-1 deficient mice and human cases of genetic HO-1 deficiency. However, the mechanism underlying the immunomodulatory actions of HO-1 remains poorly defined. This review specifically addresses macrophage polarization. The present current evidence indicates that HO-1 induction mediated by multiple pathways can drive the phenotypic shift to M2 macrophages and suggests that HO-1 induction in macrophages is a potential therapeutic approach to immunomodulation in widely diverse human diseases. (C) 2014 Elsevier Inc. All rights reserved.
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