Oxidative stress, consequences and ROS mediated cellular signaling in rheumatoid arthritis

被引:300
作者
Phull, Abdul-Rehman [1 ]
Nasir, Bakht [2 ]
ul Haq, Ihsan [2 ]
Kim, Song Ja [1 ]
机构
[1] Kongju Natl Univ, Dept Biol Sci, Coll Nat Sci, 56 Gongju Daehak Ro, Gongju Si 32588, Chungnam, South Korea
[2] Quaid I Azam Univ, Fac Biol Sci, Dept Pharm, Islamabad 45320, Pakistan
基金
新加坡国家研究基金会;
关键词
Rheumatoid arthritis; Oxidative stress; Antioxidants; Cellular signaling; NF-KAPPA-B; MITOCHONDRIAL PERMEABILITY TRANSITION; ACTIVATED PROTEIN-KINASES; NITRIC-OXIDE; HYDROGEN-PEROXIDE; SYNOVIAL-FLUID; C-JUN; NONENZYMATIC ANTIOXIDANTS; TYROSINE PHOSPHORYLATION; POSSIBLE INVOLVEMENT;
D O I
10.1016/j.cbi.2017.12.024
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
There are numerous extra- and intra-cellular processes involved in the production of reactive oxygen species (ROS). Augmented ROS generation can cause the damage of biomolecules such as proteins, nucleic acid and lipids. ROS act as an intracellular signaling component and is associated with various inflammatory responses, chronic arthropathies, including rheumatoid arthritis (RA). It is well documented that ROS can activate different signaling pathways having a vital importance in the patho-physiology of RA. Hence, understanding of the molecular pathways and their interaction might be advantageous in the development of novel therapeutic approaches for RA.
引用
收藏
页码:121 / 136
页数:16
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