Literature summary for 3.4.17.23 extracted from

Kassiri, Z.; Zhong, J.; Guo, D.; Basu, R.; Wang, X.; Liu, P.P.; Scholey, J.W.; Penninger, J.M.; Oudit, G.Y.
Loss of angiotensin-converting enzyme 2 accelerates maladaptive left ventricular remodeling in response to myocardial infarction (2009), Circ. Heart Fail., 2, 446-455.

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Natural Substrates/ Products (Substrates)

Natural Substrates	Organism	Comment (Nat. Sub.)	Natural Products	Comment (Nat. Pro.)	Rev.	Reac.
angiotensin II + H2O	Mus musculus	-	angiotensin(1-7) + L-Phe	-	?

Organism

Organism	UniProt	Comment	Textmining
Mus musculus	-	C57BL/6 wild-type mice	-

Source Tissue

Source Tissue	Comment	Organism	Textmining
heart	-	Mus musculus	-

Substrates and Products (Substrate)

Substrates	Comment Substrates	Organism	Products	Comment (Products)	Rev.	Reac.
angiotensin II + H2O	-	Mus musculus	angiotensin(1-7) + L-Phe	-	?

Synonyms

Synonyms	Comment	Organism
ACE2	-	Mus musculus

General Information

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

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Release 2023.1 (January 2023)