Oxidative Stress as an Important Contributor to the Pathogenesis of Psoriasis

Abstract

This review discusses how oxidative stress (OS), an imbalance between oxidants and antioxidants in favor of the oxidants, increased production of reactive oxygen species (ROS)/reactive nitrogen species (RNS), and decreased concentration/activity of antioxidants affect the pathogenesis or cause the enhancement of psoriasis (Ps). Here, we also consider how ROS/RNS-induced stress modulates the activity of transcriptional factors and regulates numerous protein kinase cascades that participate in the regulation of crosstalk between autophagy, apoptosis, and regeneration. Answers to these questions will likely uncover novel strategies for the treatment of Ps. Action in the field will avoid destructive effects of ROS/RNS-mediated OS resulting in cellular dysfunction and cell death. The combination of the fragmentary information on the role of OS can provide evidence to extend the full picture of Ps.

Keywords: antioxidants; oxidative stress; psoriasis; reactive oxygen species/reactive nitrogen species.

Figure 1

An oxidative stress condition typical for psoriasis. Oxidative stress leads to the overproduction of reactive oxidative species (ROS) that can damage DNA, proteins, lipids, and also results in the activation of many signaling pathways (including nuclear factor kappa-light-chain-enhancer—NF-κB and MAP kinase—mitogen-activated protein kinase), and in the stimulation of Th1 and Th17 cells and finally in the secretion of pro-inflammatory cytokines. All of this can lead to psoriatic inflammation. (JNK—c-Jun N-terminal kinase; ERK1/2—extracellular signal-regulated kinase 1/2; IFNγ—interferon γ; IL-23, IL-22, IL-17—interleukins: 23, 22, 17, respectively).