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Glucocorticoid receptors function in the pathophysiology of brain hypoxia

Gregrowicz, Jan and Rogalska, Justyna (2019) Glucocorticoid receptors function in the pathophysiology of brain hypoxia. Postępy Higieny i Medycyny Doświadczalnej, 73 . pp. 838-849. ISSN 0032-5449. https://resolver.caltech.edu/CaltechAUTHORS:20200402-091058468

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Abstract

Glucocorticoid receptors are ligand-activated transcription factors, which play an important role in the brain, mainly in stress response regulation. There are two types of receptors for glucocorticosteroids: mineralocorticoid receptors (MR) with high-affinity for the ligands and glucocorticoid receptors (GR) with a tenfold lower affinity. Selective activation of the receptors during hypoxia may decide neuronal fate, especially in the hippocampus. Depending on the severity of hypoxia-induced damage, neurons undergo necrosis or apoptosis. In the penumbral region, where neurons die mainly through the process of apoptosis, selective GR activation increases excitotoxicity, interferes with apoptotic signalling pathways and causes energy deficit in the cells, all of which promote cell death. On the other hand, selective MR activation seems to be neuroprotective. It is suggested that the main role of MR in neuroprotection is to regulate the balance between anti- and proapoptotic proteins from bcl-2 family.


Item Type:Article
Related URLs:
URLURL TypeDescription
https://doi.org/10.5604/01.3001.0013.7193DOIArticle
Additional Information:© 2019 Index Copernicus International S.A. Published: 2019-12-31. The authors have no potential conflicts of interest to declare.
Subject Keywords:glucocorticoid receptors; mineralocorticoid receptors; hypoxia; neuroprotection; apoptosis
Record Number:CaltechAUTHORS:20200402-091058468
Persistent URL:https://resolver.caltech.edu/CaltechAUTHORS:20200402-091058468
Usage Policy:No commercial reproduction, distribution, display or performance rights in this work are provided.
ID Code:102261
Collection:CaltechAUTHORS
Deposited By: Tony Diaz
Deposited On:02 Apr 2020 16:52
Last Modified:02 Apr 2020 16:52

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