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Obstructive Lung Diseases: COPD: Etiology |

The Angiotensin-Converting Enzyme 2/Angiotensin (1-7)/Mas Axis Protects Against Cigarette Smoke-Induced Apoptosis of Alveolar Epithelial Cells by Inhibiting the NOX4-Derived ROS-Mediated JNK-Bax-Caspase3 Pathway

Ting Li, MD; Xu Li, PhD; Yan Chen, MD; Miaoxia Pan, MD; Minzhou Zhang, MD; Ying Meng, PhD
Author and Funding Information

Department of Intensive Care Unit (ICU), Guangdong Provincial Hospital of Traditional Chinese Medicine, Guangzhou, China


Copyright 2016, American College of Chest Physicians. All Rights Reserved.


Chest. 2016;149(4_S):A349. doi:10.1016/j.chest.2016.02.364
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SESSION TITLE: COPD: Etiology

SESSION TYPE: Original Investigation Poster

PRESENTED ON: Saturday, April 16, 2016 at 11:45 AM - 12:45 PM

PURPOSE: Chronic obstructive pulmonary disease (COPD) is a prevalent smoking-related disease for which no disease altering therapies currently exist. The angiotensin-converting enzyme 2 (ACE2)/angiotensin (1-7) [Ang(1-7)]/Mas axis, which counteracts the angiotensin-converting enzyme (ACE)/angiotensin II (AngII)/angiotensin II type 1 receptor (AT1R) axis, has been shown to attenuate cigarette smoke-induced lung injury. Nevertheless, the exact molecular mechanism remains unclear. The present study evaluated the protective effects of the ACE2/Ang(1-7)/Mas axis on cigarette smoke-induced apoptosis of alveolar epithelial cells by inhibiting the NOX4-derived ROS-mediated JNK-Bax-caspase3 pathway.

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