Role of Reactive Oxygen Species in Inflammation: A Minireview
Inflammation is a protective response of a multicellular organism to injury in order to localize, eliminate, and remove harmful stimuli as well as to recover (or replace) damaged tissues. There recently has been increasing evidence that reactive oxygen species (ROS) are involved in the initiation, progression, and resolution of the inflammatory response. Furthermore, ROS act as microbicidal agents and second messengers in the intracellular signaling. The latter function is performed via posttranslational modification of protein- associated redox-sensitive cysteine residues that can undergo oxidation. At the same time, there is clear evidence that overproduction of ROS may result in cell and tissue injury and contribute to chronic inflammation underlying many neurodegenerative, cardiovascular, and metabolic diseases. This review has focused on the role of ROS in the key inflammatory events (increased vascular permeability and leukocyte extravasation, respiratory burst and phagocytosis, and angiogenesis) and some events leading to the resolution of inflammation. In addition, the pathological function of ROS in oxidative stress is discussed.
Keywordsreactive oxygen species inflammation oxidative stress NADPH-oxidase respiratory burst mitochondria
Unable to display preview. Download preview PDF.
- 6.Laurila, J.P., Laatikainen, L.E., Castellone, M.D., and Laukkanen, M.O., SOD3 reduces inflammatory cell migration by regulating adhesion molecule and cytokine expression, PLoS One, 2009, vol. 4, no. 6, e5786.Google Scholar
- 12.Segal, A.W., The function of the NADPH oxidase of phagocytes and its relationship to other NOXs in plants, invertebrates, and mammals, Int. J. Biochem. Cell, vol. 40, no. 4, pp. 604–618.Google Scholar
- 14.Khan, M.A. and Palaniyar, N., Transcriptional firing helps to drive NETosis, Sci. Rep., 2017, vol. 7, 41749.Google Scholar
- 15.Ikeda, S., Yamaoka-Tojo, M., Hilenski, L., Patrushev, N.A., Anwar, G.M., Quinn, M.T., and Ushio-Fukai, M., IQGAP1 regulates reactive oxygen species-dependent endothelial cell migration through interacting with Nox2, Arterioscler. Thromb. Vasc. Biol., 2005, vol. 25, no. 11, pp. 2295–2300.CrossRefGoogle Scholar
- 16.Wang, Y., Zang, Q.S., Liu, Z., Wu, Q., Maass, D., Dulan, G., Shaul, P.W., Melito, L., Frantz, D.E., Kilgore, J.A., Williams, N.S., Terada, L.S., and Nwariaku, F.E., Regulation of VEGF-induced endothelial cell migration by mitochondrial reactive oxygen species, Am. J. Physiol. Cell Physiol., 2011, vol. 301, no. 3, pp. C695–C704.Google Scholar
- 18.Kuchler, L., Giegerich, A.K., Sha, L.K., Knape, T., Wong, M.S., Schröder, K., Brandes, R.P., Heide, H., Wittig, I., Brune, B., and von Knethen, A., SYNCRIPdependent Nox2 mRNA destabilization impairs ROS formation in M2-polarized macrophages, Antioxid. Redox Signaling, 2014, vol. 21, no. 18, pp. 2483–2497.CrossRefGoogle Scholar
- 20.Tan, H.Y., Wang, N., Li, S., Hong, M., Wang, X., and Feng, Y., The reactive oxygen species in macrophage polarization: Reflecting its dual role in progression and treatment of human diseases, Oxid. Med. Cell. Longev., 2016, vol. 2016, 2795090.Google Scholar