Organism | UniProt | Comment | Textmining |
---|---|---|---|
Homo sapiens | Q9BYF1 | - |
- |
Mus musculus | Q8R0I0 | - |
- |
Source Tissue | Comment | Organism | Textmining |
---|---|---|---|
Hep-G2 cell | - |
Homo sapiens | - |
liver | - |
Mus musculus | - |
General Information | Comment | Organism |
---|---|---|
physiological function | angiotensin (1-7)/ACE2 ameliorate hepatic steatosis, oxidative stress and inflammation in free fatty acid-induced Hep-G2 cells, and Akt inhibitors reduce ACE2-mediated lipid metabolism. The ACE2-mediated Akt activation can be attenuated by blockade of ATP/P2 receptor/Calmodulin (CaM) pathway | Homo sapiens |
physiological function | deletion of ACE2 aggravates liver steatosis, which is correlated with the increased expression of hepatic lipogenic genes and the decreased expression of fatty acid oxidation-related genes in the liver of ACE2 knockout mice. Oxidative stress and inflammation are also aggravated in ACE2 knockout mice. Overexpression of ACE2 improves fatty liver in db/db mice, and the mRNA levels of fatty acid oxidation-related genes are up-regulated | Mus musculus |