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. Author manuscript; available in PMC: 2017 Jan 1.
Published in final edited form as: Transl Res. 2015 Jun 23;167(1):7–34. doi: 10.1016/j.trsl.2015.06.011

Figure 2.

Figure 2

Pivotal Functions of HO-1 in inflammation. HO-1 may have immunomodulatory effects with respect to regulating the functions of antigen presenting cells, dendritic cells, and regulatory T-cells. Heme may exert pro-inflammatory effects. HO-1 end products generated from heme degradation may modulate inflammation. Iron release from HO activity may be pro-inflammatory in the case of excess activation, and has been associated with neurodegenerative diseases. CO whether endogenously produced or applied as a pharmacological treatment, has been shown to modulate apoptotic, proliferative, and inflammatory cellular programs. In particular, CO can downregulate the production of pro-inflammatory cytokines (e.g., IL-1β, IL-6, TNFα, Mip1α/β, and upregulate the anti-inflammatory cytokines (IL-10). These effects were attributed to alterations of MAPK activities including p38 MAPK. CO can stimulate mitochondrial ROS production, which can promote the autophagy program, activate HIF-1α, and downregulate pro-inflammatory transcription factor Egr1. Recent evidence also suggests that CO can modulate the activation of the NLRP3 inflammasome, which regulates the production of IL-1β, and IL-18. BR, a product of heme degaradtion, also may exert anti-inflammatory and anti-proliferative effects.