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- W4285228927 abstract "Traumatic brain injury (TBI) is a devastating disease, where the extent of primary injury is reflected by the extent of pathophysiological processes that lead to metabolic failure, neuroinflammation, and oxidative stress. Despite advances in the knowledge of this complex pathophysiology, the underlying mechanisms have not yet been fully elucidated. Given the extent of post-traumatic changes in neuronal function and the possibility of amplifying secondary cascades, significant changes in some targets, such as Na +,K+-ATPase (an enzyme that is known to play a key role in maintaining ionic gradient) play an important role in TBI-induced pathophysiology. However, the underlying molecular mechanisms of Na+,K+-ATPase activity regulation after TBI remain largely unknown. The aim of this chapter is to evaluate the signaling cascades involved in regulating the activity of this enzyme in animal models of TBI and how this experimental data can be applied in clinical settings." @default.
- W4285228927 created "2022-07-14" @default.
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- W4285228927 date "2022-01-01" @default.
- W4285228927 modified "2023-09-26" @default.
- W4285228927 title "The role of Na+,K+-ATPase on TBI-induced physiopathology" @default.
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- W4285228927 doi "https://doi.org/10.1016/b978-0-12-823036-7.00010-4" @default.
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