NADPH Oxidase 1 and Its Derived Reactive Oxygen Species Mediated Tissue Injury and Repair
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CitationFu, Xiu-Jun, Ying-Bo Peng, Yi-Ping Hu, You-Zhen Shi, Min Yao, and Xiong Zhang. 2014. “NADPH Oxidase 1 and Its Derived Reactive Oxygen Species Mediated Tissue Injury and Repair.” Oxidative Medicine and Cellular Longevity 2014 (1): 282854. doi:10.1155/2014/282854. http://dx.doi.org/10.1155/2014/282854.
AbstractReactive oxygen species are mostly viewed to cause oxidative damage to various cells and induce organ dysfunction after ischemia-reperfusion injury. However, they are also considered as crucial molecules for cellular signal transduction in biology. NADPH oxidase, whose only function is reactive oxygen species production, has been extensively investigated in many cell types especially phagocytes. The deficiency of NADPH oxidase extends the process of inflammation and delays tissue repair, which causes chronic granulomatous disease in patients. NADPH oxidase 1, one member of the NADPH oxidase family, is not only constitutively expressed in a variety of tissues, but also induced to increase expression in both mRNA and protein levels under many circumstances. NADPH oxidase 1 and its derived reactive oxygen species are suggested to be able to regulate inflammation reaction, cell proliferation and migration, and extracellular matrix synthesis, which contribute to the processes of tissue injury and repair.
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