Oxidative stress in chronic lung disease: From mitochondrial dysfunction to dysregulated redox signaling.
Oxidative stress in chronic lung disease: From mitochondrial dysfunction to dysregulated redox signaling.
复制标题
DOI:
10.1016/j.mam.2018.08.001
复制
发表时间:
2018-10
影响因子:
10.6
通讯作者:
Anathy V
中科院分区:
文献类型:
--
作者:
van der Vliet A;Janssen-Heininger YMW;Anathy V
The lung is a delicate organ with a large surface area that is continuously exposed to the external environment, and is therefore highly vulnerable to exogenous sources of oxidative stress. In addition, each of its approximately 40 cell types can also generate reactive oxygen species (ROS), as byproducts of cellular metabolism and in a more regulated manner by NOX enzymes with functions in host defense, immune regulation, and cell proliferation or differentiation. To effectively regulate the biological actions of exogenous and endogenous ROS, various enzymatic and non-enzymatic antioxidant defense systems are present in all lung cell types to provide adequate protection against their injurious effects and to allow for appropriate ROS-mediated biological signaling. Acute and chronic lung diseases are commonly thought to be associated with increased oxidative stress, evidenced by altered cellular or extracellular redox status, increased irreversible oxidative modifications in proteins or DNA, mitochondrial dysfunction, and altered expression or activity of NOX enzymes and antioxidant enzyme systems. However, supplementation strategies with generic antioxidants has proven minimally successful in prevention or treatment of lung disease, most likely due to their inability to distinguish between harmful and beneficial actions of ROS. Recent studies have attempted to identify specific redox-based mechanisms that may mediate chronic lung disease, such as allergic asthma or pulmonary fibrosis, which provide opportunities for selective redox-based therapeutic strategies that may be useful in treatment of these diseases.
登录
查看更多内容
影响因子:
82.9
作者:
Cloonan SM;Glass K;Laucho-Contreras ME;Bhashyam AR;Cervo M;Pabón MA;Konrad C;Polverino F;Siempos II;Perez E;Mizumura K;Ghosh MC;Parameswaran H;Williams NC;Rooney KT;Chen ZH;Goldklang MP;Yuan GC;Moore SC;Demeo DL;Rouault TA;D'Armiento JM;Schon EA;Manfredi G;Quackenbush J;Mahmood A;Silverman EK;Owen CA;Choi AM
通讯作者:
Choi AM
影响因子:
4.8
作者:
Ameziane-El-Hassani, R;Morand, S;Dupuy, C
通讯作者:
Dupuy, C
影响因子:
4.8
作者:
Aracena-Parks, Paula;Goonasekera, Sanjeewa A.;Hamilton, Susan L.
通讯作者:
Hamilton, Susan L.
影响因子:
2.9
作者:
Brar, SS;Kennedy, TP;Hoidal, JR
通讯作者:
Hoidal, JR
影响因子:
4.4
作者:
Carneiro, Matheus B. H.;Roma, Eric H.;Peters, Nathan C.
通讯作者:
Peters, Nathan C.