Cigarette Smoke Causes Lung Vascular Endothelial Cell Apoptosis And Alterations Of TGF-²1 Signaling

Author(s):  
Qing Lu ◽  
Julie Newton ◽  
Min-Jong Kang ◽  
Chun Geun Lee ◽  
Jack A. Elias ◽  
...  
2021 ◽  
Vol 22 (1) ◽  
Author(s):  
Qing Song ◽  
Ping Chen ◽  
Xiang-Ming Liu

AbstractChronic obstructive pulmonary disease (COPD) is one of the most common chronic respiratory diseases with high morbidity and mortality. It has become the fifth most burdened and the third most deadly disease in the global economy and increases year by year. The prevention and treatment of COPD are urgent. Smoking is the main and most common risk factor for COPD. Cigarette smoke (CS) contains a large number of toxic substances, can cause a series of changes in the trachea, lung tissue, pulmonary blood vessels, and promotes the occurrence and development of COPD. In recent years, the development of epigenetics and molecular biology have provided new guidance for revealing the pathogenesis, diagnosis, and treatment of diseases. The latest research indicates that pulmonary vascular endothelial cell apoptosis initiates and participates in the pathogenesis of COPD. In this review, we summarize the current research on the epigenetic mechanisms and molecular biology of CS-induced pulmonary vascular endothelial cell apoptosis in COPD, providing a new research direction for pathogenesis of COPD and a new target for the diagnosis, treatment, and prevention of COPD.


2018 ◽  
Vol 38 (3) ◽  
Author(s):  
Chengfu Song ◽  
Xiangdong Zhao

In patients with cerebral infarction (CI), elevated serum uric acid (UA) level may exacerbate the occurrence and development of carotid atherosclerosis (AS). Our study intended to explore the underlying mechanism. We enrolled 86 patients with CI, and divided them into four groups: Non-AS, AS-mild, AS-moderate, and AS-severe groups; the levels of UA and oxidative stress-related factors in serum were detected. The middle cerebral artery occlusion (MCAO) model was used to stimulate CI in rats, and different doses of UA were administrated. The levels of oxidative stress-related factors in serum were detected. Hematoxylin & eosin (H&E) staining was used to observe the morphological alterations, and the apoptotic cell death detection kit was used to detect apoptotic cells. Increased UA concentration and enhanced oxidative stress were found in AS patients. H&E staining results showed that UA treatment exacerbated morphological damage in rats with MCAO, promoted oxidative stress, and enhanced vascular endothelial cell apoptosis in rats with MCAO.


2006 ◽  
Vol 54 (4) ◽  
pp. 268-274 ◽  
Author(s):  
Min Xiang ◽  
Min Yang ◽  
Chenghua Zhou ◽  
Juan Liu ◽  
Wenna Li ◽  
...  

2000 ◽  
Vol 35 (7) ◽  
pp. 1785-1790 ◽  
Author(s):  
Atsushi Iwakura ◽  
Masatoshi Fujita ◽  
Koji Hasegawa ◽  
Tatsuya Sawamura ◽  
Ryuji Nohara ◽  
...  

Sign in / Sign up

Export Citation Format

Share Document