Table 1.
Upregulation of heme oxygenase-1 in donor liver to alleviate ischemia-reperfusion injury and rejection
| Effective product | Targets | Results | Ref. |
| HO-1 | KC | Preventing IRI | [4] |
| HO-1 | Attenuating apoptosis of SEC | Alleviating IRI | [5] |
| HO-1 | Inhibiting DC maturation | Reducing rejection | [6] |
| HO-1 | Anti-inflammatory differentiation of KC | Preventing IRI | [24] |
| HO-1 | Modulating oxidative stress and proinflammatory mediators | Alleviating IRI | [30] |
| CO | Suppressing T cell proliferation | Reducing rejection | [31] |
| HO-1 | Microchimerism | Inducing allograft tolerance | [41] |
| CO | Inhibiting TLR-induced DC maturation | Reducing rejection | [42] |
| HO-1 | Suppressing intragraft infiltration of KC and neutrophils, preventing proinflammatory cytokine and chemokine expression | Alleviating IRI | [50] |
| HO-1 | Inducing Treg | Inducing allograft tolerance | [56] |
| Biliverdin | Decreasing P-selectin, ICAM-1, iNOS and IL-6 | Alleviating IRI | [60] |
HO-1: Heme oxygenase 1; CO: Carbon monoxide; KC: Kupffer cell; SEC: Sinusoidal endothelial cell; DC: Dendritic cell; TLR: Toll-like receptor; Treg: Regulatory T cells; ICAM-1: Intercellular adhesion molecule-1; iNOS: Inducible nitric oxide synthase; IL: Interleukin; IRI: Ischemia-reperfusion injury.