Natural Substrates | Organism | Comment (Nat. Sub.) | Natural Products | Comment (Nat. Pro.) | Rev. | Reac. |
---|---|---|---|---|---|---|
angiotensin II + H2O | Mus musculus | - |
angiotensin(1-7) + L-Phe | - |
? |
Organism | UniProt | Comment | Textmining |
---|---|---|---|
Mus musculus | - |
C57BL/6 wild-type mice | - |
Source Tissue | Comment | Organism | Textmining |
---|---|---|---|
heart | - |
Mus musculus | - |
Substrates | Comment Substrates | Organism | Products | Comment (Products) | Rev. | Reac. |
---|---|---|---|---|---|---|
angiotensin II + H2O | - |
Mus musculus | angiotensin(1-7) + L-Phe | - |
? |
Synonyms | Comment | Organism |
---|---|---|
ACE2 | - |
Mus musculus |
General Information | Comment | Organism |
---|---|---|
malfunction | loss of ACE2 accelerates maladaptive left ventricular remodeling in response to myocardial infarction, MI, overview. ACE2 deficiency leads to increased matrix metalloproteinases 2 and 9 levels with MMP2 activation in the infarct and peri-infarct regions, as well as increased gelatinase activity leading to a disrupted extracellular matrix structure after MI. Loss of ACE2 also leads to increased neutrophilic infiltration in the infarct and peri-infarct regions, resulting in upregulation of inflammatory cytokines, interferon-gamma, interleukin-6, and the chemokine, monocyte chemoattractant protein-1, as well as increased phosphorylation of ERK1/2 and JNK1/2 signaling pathways | Mus musculus |
physiological function | ACE2 is a monocarboxypeptidase that metabolizes Ang II into Ang 1-7, thereby functioning as a negative regulator of the renin-angiotensin system | Mus musculus |