The effect of phosphatidylinositol-3 kinase inhibition on matrix metalloproteinase-9 and reactive oxygen species release from chronic obstructive pulmonary disease neutrophils

2016 ◽  
Vol 35 ◽  
pp. 155-162 ◽  
Author(s):  
V. Gupta ◽  
A. Khan ◽  
A. Higham ◽  
J. Lemon ◽  
S. Sriskantharajah ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Chronic Obstructive Pulmonary Disease ◽  
Matrix Metalloproteinase ◽  
Pulmonary Disease ◽  
Reactive Oxygen ◽  
Chronic Obstructive ◽  
Oxygen Species ◽  
Phosphatidylinositol 3 Kinase ◽  
Obstructive Pulmonary Disease ◽  
Metalloproteinase 9

scholarly journals Reactive Oxygen Species and Antioxidative Defense in Chronic Obstructive Pulmonary Disease

Antioxidants ◽  
2021 ◽  
Vol 10 (10) ◽  
pp. 1537
Author(s):  
Akihiko Taniguchi ◽  
Mitsuru Tsuge ◽  
Nobuaki Miyahara ◽  
Hirokazu Tsukahara
Keyword(s):  
Oxidative Stress ◽  
Reactive Oxygen Species ◽  
Chronic Obstructive Pulmonary Disease ◽  
Pulmonary Disease ◽  
Reactive Oxygen ◽  
Chronic Obstructive ◽  
Oxygen Species ◽  
Antioxidative Defense ◽  
Obstructive Pulmonary Disease ◽  
Antioxidative Therapy

The respiratory system is continuously exposed to endogenous and exogenous oxidants. Chronic obstructive pulmonary disease (COPD) is characterized by chronic inflammation of the airways, leading to the destruction of lung parenchyma (emphysema) and declining pulmonary function. It is increasingly obvious that reactive oxygen species (ROS) and reactive nitrogen species (RNS) contribute to the progression and amplification of the inflammatory responses related to this disease. First, we described the association between cigarette smoking, the most representative exogenous oxidant, and COPD and then presented the multiple pathophysiological aspects of ROS and antioxidative defense systems in the development and progression of COPD. Second, the relationship between nitric oxide system (endothelial) dysfunction and oxidative stress has been discussed. Third, we have provided data on the use of these biomarkers in the pathogenetic mechanisms involved in COPD and its progression and presented an overview of oxidative stress biomarkers having clinical applications in respiratory medicine, including those in exhaled breath, as per recent observations. Finally, we explained the findings of recent clinical and experimental studies evaluating the efficacy of antioxidative interventions for COPD. Future breakthroughs in antioxidative therapy may provide a promising therapeutic strategy for the prevention and treatment of COPD.

scholarly journals Iron-Regulated Reactive Oxygen Species Production and Programmed Cell Death in Chronic Obstructive Pulmonary Disease

Antioxidants ◽  
2021 ◽  
Vol 10 (10) ◽  
pp. 1569
Author(s):  
Kenji Mizumura ◽  
Yasuhiro Gon
Keyword(s):  
Reactive Oxygen Species ◽  
Chronic Obstructive Pulmonary Disease ◽  
Cell Death ◽  
Programmed Cell Death ◽  
Pulmonary Disease ◽  
Iron Metabolism ◽  
Reactive Oxygen ◽  
Chronic Obstructive ◽  
Oxygen Species ◽  
Obstructive Pulmonary Disease

Chronic obstructive pulmonary disease (COPD) is characterized by persistent respiratory symptoms and airflow limitation. However, the pathogenesis of COPD remains unclear. Currently, it is known to involve the loss of alveolar surface area (emphysema) and airway inflammation (bronchitis), primarily due to exposure to cigarette smoke (CS). CS causes epithelial cell death, resulting in pulmonary emphysema. Moreover, CS induces iron accumulation in the mitochondria and cytosol, resulting in programmed cell death. Although apoptosis has long been investigated as the sole form of programmed cell death in COPD, accumulating evidence indicates that a regulated form of necrosis, called necroptosis, and a unique iron-dependent form of non-apoptotic cell death, called ferroptosis, is implicated in the pathogenesis of COPD. Iron metabolism plays a key role in producing reactive oxygen species (ROS), including mitochondrial ROS and lipid peroxidation end-products, and activating both necroptosis and ferroptosis. This review outlines recent studies exploring CS-mediated iron metabolism and ROS production, along with the regulation of programmed cell death in COPD. Elucidating the mechanisms of these pathways may provide novel therapeutic targets for COPD.

scholarly journals Reactive Oxygen Species in Chronic Obstructive Pulmonary Disease

2018 ◽  
Vol 2018 ◽  
pp. 1-9 ◽  
Author(s):  
Samia Boukhenouna ◽  
Mark A. Wilson ◽  
Karim Bahmed ◽  
Beata Kosmider
Keyword(s):  
Reactive Oxygen Species ◽  
Chronic Obstructive Pulmonary Disease ◽  
Disease Progression ◽  
Pulmonary Disease ◽  
Cell Injury ◽  
Reactive Oxygen ◽  
Chronic Obstructive ◽  
Oxygen Species ◽  
Obstructive Pulmonary Disease ◽  
Antioxidant Defense Systems

Chronic obstructive pulmonary disease (COPD) includes chronic bronchitis and emphysema. Environmental exposure, primarily cigarette smoking, can cause high oxidative stress and is the main factor of COPD development. Cigarette smoke also contributes to the imbalance of oxidant/antioxidant due to exogenous reactive oxygen species (ROS). Moreover, endogenously released ROS during the inflammatory process and mitochondrial dysfunction may contribute to this disease progression. ROS and reactive nitrogen species (RNS) can oxidize different biomolecules such as DNA, proteins, and lipids leading to epithelial cell injury and death. Various detoxifying enzymes and antioxidant defense systems can be involved in ROS removal. In this review, we summarize the main findings regarding the biological role of ROS, which may contribute to COPD development, and cytoprotective mechanisms against this disease progression.

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