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. 2009 Jul 17;41(3):251–260. doi: 10.1165/rcmb.2009-0170TR

TABLE 1.

THERAPEUTIC APPLICATIONS OF HO-1 END-PRODUCTS

Molecule Injury/Disease Model Protection Phenotype References
Carbon monoxide (gas) Systemic endotoxemia (mice) Decreased proinflammatory cytokine production 25
Hyperoxia-induced acute lung injury (mice) Decreased proinflammatory cytokine production, increased survival 99, 106
Lung ischemia/reperfusion injury (mice) Reduced apoptosis 107
Ventilator-induced lung injury (rats and mice) Decreased proinflammatory cytokine production 4, 94, 108
Vascular injury (rats and mice) Reduced inflammation, inhibition of vascular smooth muscle proliferation 26
Pulmonary hypertension (rat) Inhibition of smooth muscle proliferation, increased smooth muscle apoptosis 109
Cytokine-induced liver injury (mice) Organ preservation, reduced apoptosis 120
Organ transplantation (lung, heart, liver, kidney, small intestinal) (rat) Decreased inflammation, apoptosis, reduced graft rejection 12, 110114, 121
Systemic endotoxemia (pigs) Improved organ function, decreased proinflammatory cytokine production 122
Carbon monoxide (CORM) Systemic endotoxemia (mice) Decreased inflammation 123
Organ transplantation Improved organ function 124
Biliverdin/Bilirubin Vascular Injury (rats) Inhibition of smooth muscle proliferation 115
Transplantation (rats) Decreased inflammation, apoptosis, reduced graft rejection 113, 2729