Advances of endoplasmic reticulum stress in acute respiratory distress syndrome.
10.3760/cma.j.issn.2095-4352.2019.12.026
- Author:
Fei HE
1
;
Nan CAI
1
;
Jun WANG
1
;
Chao WU
2
Author Information
1. Department of Critical Care Medicine, the Second Affiliated Hospital of Kunming Medical University, Kunming 650000, Yunnan, China.
2. Department of Infectious Disease, Nanjing Drum Tower Hospital, Nanjing University Medical School, Nanjing 210008, Jiangsu, China. Corresponding author: Wu Chao, Email: chaowu_62@sina.com.
- Publication Type:Journal Article
- MeSH:
Apoptosis;
Endoplasmic Reticulum Stress;
Humans;
Lung;
Pulmonary Edema;
Respiratory Distress Syndrome
- From:
Chinese Critical Care Medicine
2019;31(12):1552-1554
- CountryChina
- Language:Chinese
-
Abstract:
Acute respiratory distress syndrome (ARDS) is an acute pulmonary edema induced by non-cardiac factors and a clinical syndrome characterized by respiratory distress and refractory hypoxemia. The pathogenesis of ARDS is complex. Systemic or local damaging factors can aggravate the inflammatory injury of lung tissue dependent on the activation of endoplasmic reticulum stress (ERs) and unfolded protein responses (UPR) and correlation with various damaging mechanisms such as inflammatory response, oxidative stress, apoptosis, autophagy, and calcium homeostasis. This article reviews the progress of ERs associated with ARDS to help us understand the pathogenesis of ARDS.
