Journal List > Hanyang Med Rev > v.33(2) > 1044178

This article has been corrected. See "Erratum: Role of Reactive Oxygen Species in Cell Death Pathways" in Volume 33 on page 185.
Kang: Role of Reactive Oxygen Species in Cell Death Pathways

Abstract

Reactive oxygen species (ROS) are the chemical species that includes the superoxide anion, hydrogen peroxide and hydrogen radical. These ROS are simply thought as a group of molecules harmful to cells because they oxidize proteins, lipids and DNA, and they mediate cell death including apoptosis or necrosis. On the other hand, ROS have been shown to act as essential intracellular second messengers for certain cytokines and growth factors. Although the importance of ROS in the execution of cell death is controversial, ROS are likely to be involved in the signal transduction mechanism for cell death as signaling intermediates in death receptor initiated signaling pathways, specifically in the tumor necrosis factor alpha-tumor necrosis factor receptor 1 (TNFα-TNFR1) pathway. In this review, using TNFα-TNFR as the model system, we attempt to address the involvement of intracellular ROS in TNFα induced cell death, including apoptosis, necrosis and an alternative form of programmed cell death, necroptosis.

Figures and Tables

Fig. 1
TNFα induced formation of apoptotic and necroptotic signaling complexes. TNFR1, tumor necrosis factor receptor 1; TRADD, TNFR type 1-associated death domain protein; TRAF2, TNF receptor-associated factor 2; cIAP1, cellular inhibitor of apoptosis 1; JNK, c-Jun N-terminal kinase; RIP1, receptor-interacting protein 1; FADD, Fas-associated death domain; GSH, glutathione; MnSOD, manganese-dependent superoxide dismutase; PRx, peroxiredoxin-3; NF-κB, nuclear factor kappa-light-chain-enhancer of activator B cells; ROS, reactive oxygen species.
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