Mitochondrial dysfunction and biological therapy: a new look at rheumatoid arthritis

Abstract

A marked increase in interest towards the mitochondria and their implication into the pathogenesis of various immune-mediated diseases is observed. A multitude of studies are establishing the mitochondrial dysfunction and it's pathophysiological sequelae as key events, contributing to the progression of rheumatoid arthritis. The oxidative stress and release of mitochondrial molecules into the intra- and extracelular compartments are a result of the loss of function and integrity of the mitochondria. Some biomarkers, which accurately reflect the state of oxidative stress in rheumatoid arthritis patients, have been successfuly identified. The change in the levels of those markers as a result of treatment with biologic DMARDs (bDMARDs) has been analyzed. However, there is still insufficient data regarding the effect of the target-synthetic DMARDs (tsDMARDs) on the oxidative stress.