The effect of TALDO1 depletion on NADPH and GSH is discordant among various cells. Suppression of TALDO1 increases NADPH and GSH production and enhances oxidative stress in human Jurkat and H9 T cells, however; TALDO1 deficiency diminishes NADPH and GSH production in human lymphoblasts,. The upregulation of TALDO1 in CDPSCs may increase NADPH and GSH expression, which may contribute to protecting CDPSCs from oxidative damage. GLRX3, an essential binding protein, has been reported to play important roles in various signaling pathways including embryogenesis, immune cell response, the regulation of cardiac hypertrophy, cancer cell functions and iron homeostasis,. GLRX3 is necessary to protect cells against oxidative stress and GLRX3 deletion leads to embryonic lethality in mice. The pulp with deep caries is more likely to suffer from oxidative stress. The up-regulation of GLRX3 in CDPSCs may help protect them from being damaged by reactive oxygen species. APEH belongs to the prolyl oligopeptidase family of serine proteases. Previous studies have showed that APEH contributes to the elimination of the oxidized proteins in mammalian cells and in plants. APEH may be a potential regulator in sustaining the homeostasis of the cytoplasmic antioxidative system. The expression of APEH should be enhanced in CDPSCs, as dental pulp with deep caries is more susceptible to oxidized stress; however, our proteomic analysis showed opposite results. The antioxidative role of APEH in CDPSCs requires further investigation. HSP90AA1 is a highly conserved and abundant protein. It has been implicated in the activation of various proteins such as important mediators of signal transduction, cell cycle regulation, differentiation and pathogenic factors involved in tumor progression. Previous studies showed that HSP90AA1 played an important role in infectious disease by interacting with various bacterial and viral proteins. Moreover, HSP90AA1 is unregulated under elevated temperature. Two reasons may be accountable for the up-regulation of HSP90AA1 in CDPSCs. First, the by-products secreted by bacteria and viruses might enhance the expression level of HSP90AA1 in stem cells isolated from dental pulp undergoing stimulation from a deep carious lesion. Moreover, the fluctuating oral temperature may increase HSP90AA1 expression in CDPSCs, as dental pulp with deep caries is more vulnerable to temperature stimuli without sufficent hard dental tissue protection. Isocitrate dehydrogenase catalyzes the oxidative decarboxylation of isocitrate to form a-ketoglutarate. This process is considered to be one of the key enzymes in the tricarboxylic acid cycle. In mammals, there are three types of isoenzymes represented by cytosolic NADP-specific IDH, mitochondrial NADP-specific IDH, and mitochondrial NADspecific IDH.