Role of mTORC1 Controlling Proteostasis after Brain Ischemia

Frontiers in Neuroscience
Maria Jose Pérez-ÁlvarezFrancisco Wandosell

Abstract

Intense efforts are being undertaken to understand the pathophysiological mechanisms triggered after brain ischemia and to develop effective pharmacological treatments. However, the underlying molecular mechanisms are complex and not completely understood. One of the main problems is the fact that the ischemic damage is time-dependent and ranges from negligible to massive, involving different cell types such as neurons, astrocytes, microglia, endothelial cells, and some blood-derived cells (neutrophils, lymphocytes, etc.). Thus, approaching such a complicated cellular response generates a more complex combination of molecular mechanisms, in which cell death, cellular damage, stress and repair are intermixed. For this reason, animal and cellular model systems are needed in order to dissect and clarify which molecular mechanisms have to be promoted and/or blocked. Brain ischemia may be analyzed from two different perspectives: that of oxygen deprivation (hypoxic damageper se) and that of deprivation of glucose/serum factors. For investigations of ischemic stroke, middle cerebral artery occlusion (MCAO) is the preferredin vivomodel, and uses two different approaches: transient (tMCAO), where reperfusion is permitted; or permanent ...Continue Reading

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Citations

Jul 30, 2020·International Journal of Molecular Sciences·Tiffany J Rios-FullerRobert J Schneider
Oct 3, 2018·Journal of Molecular Neuroscience : MN·Lu-Yao AoYun-Man Li
Aug 27, 2019·Frontiers in Immunology·Mark R ZielinskiNoel R Rose
Dec 31, 2020·International Journal of Molecular Sciences·Erzsébet KövesdiIstván M Abrahám
Jan 26, 2021·BioMed Research International·Houxi XuShuping Fu
Jan 29, 2021·Oxidative Medicine and Cellular Longevity·Hongyu ChenBin Zhao
Apr 29, 2021·Neural Regeneration Research·Mario Villa Gonzalez, Maria José Pérez-Álvarez

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Methods Mentioned

BETA
transgenic
GTPase
ubiquitination

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