Application | Comment | Organism |
---|---|---|
medicine | the enzyme is a target in treatment of cardiomyopathy | Mus musculus |
Protein Variants | Comment | Organism |
---|---|---|
additional information | generation of Alox15-deficient (12/15-LOX KO) mice | Mus musculus |
Inhibitors | Comment | Organism | Structure |
---|---|---|---|
cinnamyl-3,4-dihydroxy-cyanocinnamate | - |
Mus musculus |
Natural Substrates | Organism | Comment (Nat. Sub.) | Natural Products | Comment (Nat. Pro.) | Rev. | Reac. |
---|---|---|---|---|---|---|
arachidonate + O2 | Mus musculus | - |
(5Z,8Z,11Z,13E)-(15S)-15-hydroperoxyicosa-5,8,11,13-tetraenoate | - |
? | |
arachidonate + O2 | Mus musculus C57BL/6 | - |
(5Z,8Z,11Z,13E)-(15S)-15-hydroperoxyicosa-5,8,11,13-tetraenoate | - |
? |
Organism | UniProt | Comment | Textmining |
---|---|---|---|
Mus musculus | P39654 | - |
- |
Mus musculus C57BL/6 | P39654 | - |
- |
Source Tissue | Comment | Organism | Textmining |
---|---|---|---|
cardiomyocyte | - |
Mus musculus | - |
heart | expression of 12/15-LOX pathway is upregulated in the diabetic heart | Mus musculus | - |
Substrates | Comment Substrates | Organism | Products | Comment (Products) | Rev. | Reac. |
---|---|---|---|---|---|---|
arachidonate + O2 | - |
Mus musculus | (5Z,8Z,11Z,13E)-(15S)-15-hydroperoxyicosa-5,8,11,13-tetraenoate | - |
? | |
arachidonate + O2 | - |
Mus musculus C57BL/6 | (5Z,8Z,11Z,13E)-(15S)-15-hydroperoxyicosa-5,8,11,13-tetraenoate | - |
? |
Synonyms | Comment | Organism |
---|---|---|
12/15-LOX | - |
Mus musculus |
Alox15 | - |
Mus musculus |
arachidonate 12/15-lipoxygenase | - |
Mus musculus |
cardiac 12/15-LOX | - |
Mus musculus |
Organism | Comment | Expression |
---|---|---|
Mus musculus | expression of 12/15-LOX pathway is upregulated in the diabetic heart | up |
General Information | Comment | Organism |
---|---|---|
malfunction | streptozotocin (STZ)-induced diabetic mice show upregulated expression of 12/15-LOX and inflammatory cytokines such as tumor necrosis factor (TNF)-alpha and nuclear factor (NF)-kappaB in diabetic hearts. Disruption of 12/15-LOX significantly improves STZ-induced cardiac dysfunction and fibrosis. Deletion of 12/15-LOX inhibits the increases of TNF-alpha and NF-kappaB as well as the production of STZ-induced reactive oxygen species in the heart. Administration of N-acetylcysteine in diabetic mice prevents STZ-induced cardiac fibrosis. Neonatal cultured cardiomyocytes exposed to high glucose conditions induce the expression of 12/15-LOX as well as TNF-alpha, NF-kappaB, and collagen markers. These increases are inhibited by treatment of the 12/15-LOX inhibitor. Disruption of 12/15-LOX reduces inflammation, oxidative stress, and fibrosis in the diabetic heart, thereby improving systolic dysfunction. Disruption of 12/15-LOX decreases cardiac inflammation induced by hyperglycemia | Mus musculus |
metabolism | cardiac 12/15-LOX pathway induced by high glucose condition increases the expression of cardiac inflammation in vitro | Mus musculus |
physiological function | cardiac 12/15-LOX-induced inflammation and oxidative stress are involved in the development of diabetic cardiomyopathy. 12/15-LOX induces cardiac oxidative stress in the diabetic heart | Mus musculus |