Angiotensin-Converting Enzyme 2 Inhibits Apoptosis of Pulmonary Endothelial Cells During Acute Lung Injury Through Suppressing MiR-4262
Author(s) -
Hong Bao,
Fengying Gao,
Guogang Xie,
Zhenwei Liu
Publication year - 2015
Publication title -
cellular physiology and biochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.486
H-Index - 87
eISSN - 1421-9778
pISSN - 1015-8987
DOI - 10.1159/000430393
Subject(s) - downregulation and upregulation , apoptosis , western blot , angiotensin converting enzyme 2 , lung , medicine , angiotensin ii , messenger rna , bleomycin , microbiology and biotechnology , andrology , biology , endocrinology , gene , blood pressure , biochemistry , chemotherapy , infectious disease (medical specialty) , disease , covid-19
Angiotensin converting enzyme 2 (ACE2) treatment suppresses the severity of acute lung injury (ALI). The effects of ACE2 in ALI have been shown to not only result from its antagonizing hydrolyzing angiotensin II (AngII), which is responsible for reduction in the vascular tension and pulmonary accumulation of inflammatory cells, but also result from a role of ACE2 in suppressing the ALI-induced apoptosis of pulmonary endothelial cells (PECs). Nevertheless, the underlying mechanisms of the role of ACE2 on PEC apoptosis are not completely understood.
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