About this Research Topic
Oxidative stress is one of the main hallmarks of different pathologies processes. Oxidative stress can damage important cell components, including proteins, nucleic acids, lipids and membranes, leading to a dysfunction of homeostasis and normal cell functioning. In order to prevent the increase of free radicals, cells have developed a large range of defense mechanisms. The transcription factor Nrf2 (nuclear factor erythroid 2–related factor 2) is a master regulator of cellular resistance to oxidants and inflammation due to regulation of transcription and expression of inducible antioxidant elements (phase II antioxidant enzymes, reductases, drug transporters, among others) in response to oxidative damage. These proteins are able to scavenge free radicals directly or indirectly, and finally reduce the burden of cellular oxidative stress. A number of studies have focused in the protective mechanisms mediated by Nrf2 and it have been described novel compounds targeting Nrf2. Nrf2 activation protects against oxidative damage produced by inflammation as a result of acute injuries, drugs, exogenous agents and many other stimuli. Therefore, there is a growing interest in the relation between Nrf2 and disease and the identification of novel approaches targeting Nrf2 pathway to prevent and/or retard tissue injury. There are several on-going clinical trials assessing Nrf2-based therapies for the treatment cardiovascular, neurological and renal diseases, among others.
Keywords: Nrf2, oxidation, inflammation, disease, injury
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