Oxidation in rheumatoid arthritis

[Guest guest]

[The existence of oxidative processes hints that anti-oxidant therapy

may have benefits for inflammatory types of arthritis - David]

 

Review

Oxidation in rheumatoid arthritis

Carol A Hitchon and Hani S El-Gabalawy

http://arthritis-research.com/content/ar1447/abstract

 

Arthritis Res Ther 2004, 6:265-278 doi:10.1186/ar1447

 

Published 13 October 2004

 

Abstract (provisional)

 

Oxygen metabolism plays an important role in the pathogenesis of

rheumatoid arthritis. Reactive oxygen species (ROS) produced in the

course of cellular oxidative phosphorylation, and by activated

phagocytic cells during oxidative bursts, exceed the physiological

buffering capacity and results in oxidative stress. The excessive

production of ROS can damage protein, lipids, nucleic acids, and matrix

components. They also serve as important intracellular signaling

molecules that amplify the synovial inflammatory-proliferative response.

Repetitive cycles of hypoxia/reoxygenation associated with changes in

synovial perfusion are postulated to activate hypoxia inducible factor-1

alpha (HIF-1alpha) and nuclear factor- kappa B (NF-kappaB), two key

transcription factors that are regulated by changes in cellular

oxygentation and cytokine stimulation, and that in turn orchestrate the

expression of a spectrum of genes that are critical to the persistence

of synovitis. An understanding of the complex interactions involved in

these pathways may allow the development of novel therapeutic strategies

for RA.