Summary

HMOX1 is important for producing an enzyme that helps combat free radicals.

Enhanced production may contribute to disease as well by depositing too much iron (R).

Impaired HMOX1 activity could reduce the neuronal production of biliverdin/bilirubin metabolites, which exert an antioxidant role (R).

HMOX1 is a gene that produces the enzyme Heme oxygenase-1 (HO-1). Heme oxygenase-1 (HO-1) is an enzyme that helps degrade heme into biliverdin, iron, and carbon monoxide (R). HO-1 was suggested to have an anti-oxidative stress, anti-inflammatory, and anti-cancer effect.  It helps protect cells from dying as well.  

The mechanisms are via carbon monoxide, biliverdin, and iron (R). Heme oxygenase is induced by oxidative stress, and in animal models increasing this gene expression seems to be protective (R). Carbon monoxide released from heme oxygenase reactions can relax blood vessels independently or influence the function of nitric oxide synthesis (R).

Enhanced production may contribute to disease as well by depositing too much iron (R).

Impaired HMOX1 activity could reduce the neuronal production of biliverdin/bilirubin metabolites, which exert an antioxidant role (R).

HO-1 is essential for heme degradation by producing bile pigments, ferritin, and carbon monoxide (R). HO-1 helps close tight junctions to help with leaky gut. HO-1 increases IFNb (R), Bilirubin(R), Carbon Monoxide, IL-10 and IL-1a (R).

Heme oxygenase cleaves the heme ring at the alpha methene bridge to form biliverdin. Biliverdin is subsequently converted to bilirubin by biliverdin reductase. Under physiological conditions, the activity of heme oxygenase is highest in the spleen, where senescent erythrocytes are sequestrated and destroyed. Exhibits cytoprotective effects since excess of free heme sensitizes cells to undergo apoptosis.

Heme oxygenase 1 deficiency (HMOX1D): A disease characterized by impaired stress hematopoiesis, resulting in marked erythrocyte fragmentation and intravascular hemolysis, coagulation abnormalities, endothelial damage, and iron deposition in renal and hepatic tissues. Clinical features include persistent hemolytic anemia, asplenia, nephritis, generalized erythematous rash, growth retardation and hepatomegaly. [MIM:614034]

     From NCBI Gene: Heme oxygenase, an essential enzyme in heme catabolism, cleaves heme to form biliverdin, which is subsequently converted to bilirubin by biliverdin reductase, and carbon monoxide, a putative neurotransmitter. Heme oxygenase activity is induced by its substrate heme and by various nonheme substances. Heme oxygenase occurs as 2 isozymes, an inducible heme oxygenase-1 and a constitutive heme oxygenase-2. HMOX1 and HMOX2 belong to the heme oxygenase family. [provided by RefSeq, Jul 2008] From UniProt: Heme oxygenase cleaves the heme ring at the alpha methene bridge to form biliverdin. Biliverdin is subsequently converted to bilirubin by biliverdin reductase. Under physiological conditions, the activity of heme oxygenase is highest in the spleen, where senescent erythrocytes are sequestrated and destroyed. Exhibits cytoprotective effects since excess of free heme sensitizes cells to undergo apoptosis.


It's better to have this gene increased most of the time.

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