Literature summary for 3.4.17.23 extracted from

Li, Y.; Zeng, Z.; Cao, Y.; Liu, Y.; Ping, F.; Liang, M.; Xue, Y.; Xi, C.; Zhou, M.; Jiang, W.
Angiotensin-converting enzyme 2 prevents lipopolysaccharide-induced rat acute lung injury via suppressing the ERK1/2 and NF-kappaB signaling pathways (2016), Sci. Rep., 6, 27911 .

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Organism

Organism	UniProt	Comment	Textmining
Rattus norvegicus	Q5EGZ1	-	-

Source Tissue

Source Tissue	Comment	Organism	Textmining
lung	-	Rattus norvegicus	-

General Information

General Information	Comment	Organism
physiological function	lipopolysaccharide-induced lung injury and inflammatory response are significantly prevented by ACE2 overexpression in lung and deteriorated by Ace2 shRNA. Mas receptor antagonist A779 or ACE2 inhibitor MLN-4760 pretreatment abolish the protective effects of ACE2. Overexpression of ACE2 significantly reduces the angiotensin II/angiotensin -(1-7) ratio in broncho-alveolar lavage fluid and up-regulated Mas mRNA expression in lung. The blockade of ACE2 on lipopolysaccharide-induced phosphorylation of ERK1/2, p38 and p50/p65 is also abolished by A779. Only the ERK1/2 inhibitor significantly attenuates lung injury in ACE2 overexpressing rats pretreated with A779	Rattus norvegicus

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Release 2023.1 (January 2023)