Neurodegeneration: Keeping ATF4 on a Tight Leash
Activation of the endoplasmic reticulum (ER) stress and ER stress response, also known as the unfolded protein response (UPR), is common to various degenerative disorders. Therefore, signaling components of the UPR are currently emerging as potential targets for intervention and treatment of human d...
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| Format: | Article |
| Language: | English |
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Frontiers Media S.A.
2017-12-01
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| Series: | Frontiers in Cellular Neuroscience |
| Subjects: | |
| Online Access: | http://journal.frontiersin.org/article/10.3389/fncel.2017.00410/full |
| _version_ | 1819058727903297536 |
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| author | Priyamvada M. Pitale Oleg Gorbatyuk Oleg Gorbatyuk Marina Gorbatyuk |
| author_facet | Priyamvada M. Pitale Oleg Gorbatyuk Oleg Gorbatyuk Marina Gorbatyuk |
| author_sort | Priyamvada M. Pitale |
| collection | DOAJ |
| description | Activation of the endoplasmic reticulum (ER) stress and ER stress response, also known as the unfolded protein response (UPR), is common to various degenerative disorders. Therefore, signaling components of the UPR are currently emerging as potential targets for intervention and treatment of human diseases. One UPR signaling member, activating transcription factor 4 (ATF4), has been found up-regulated in many pathological conditions, pointing to therapeutic potential in targeting its expression. In cells, ATF4 governs multiple signaling pathways, including autophagy, oxidative stress, inflammation, and translation, suggesting a multifaceted role of ATF4 in the progression of various pathologies. However, ATF4 has been shown to trigger both pro-survival and pro-death pathways, and this, perhaps, can explain the contradictory opinions in current literature regarding targeting ATF4 for clinical application. In this review, we summarized recent published studies from our labs and others that focus on the therapeutic potential of the strategy controlling ATF4 expression in different retinal and neurodegenerative disorders. |
| first_indexed | 2024-12-21T13:59:48Z |
| format | Article |
| id | doaj.art-68f68e9cce6f4522acaa724002e29ee4 |
| institution | Directory Open Access Journal |
| issn | 1662-5102 |
| language | English |
| last_indexed | 2024-12-21T13:59:48Z |
| publishDate | 2017-12-01 |
| publisher | Frontiers Media S.A. |
| record_format | Article |
| series | Frontiers in Cellular Neuroscience |
| spelling | doaj.art-68f68e9cce6f4522acaa724002e29ee42022-12-21T19:01:24ZengFrontiers Media S.A.Frontiers in Cellular Neuroscience1662-51022017-12-011110.3389/fncel.2017.00410312888Neurodegeneration: Keeping ATF4 on a Tight LeashPriyamvada M. Pitale0Oleg Gorbatyuk1Oleg Gorbatyuk2Marina Gorbatyuk3Department of Optometry and Vision Science, School of Optometry, University of Alabama at Birmingham, Birmingham, AL, United StatesDepartment of Optometry and Vision Science, School of Optometry, University of Alabama at Birmingham, Birmingham, AL, United StatesDepartment of Neurology, Center for Neurodegeneration and Experimental Therapeutics, University of Alabama at Birmingham, Birmingham, AL, United StatesDepartment of Optometry and Vision Science, School of Optometry, University of Alabama at Birmingham, Birmingham, AL, United StatesActivation of the endoplasmic reticulum (ER) stress and ER stress response, also known as the unfolded protein response (UPR), is common to various degenerative disorders. Therefore, signaling components of the UPR are currently emerging as potential targets for intervention and treatment of human diseases. One UPR signaling member, activating transcription factor 4 (ATF4), has been found up-regulated in many pathological conditions, pointing to therapeutic potential in targeting its expression. In cells, ATF4 governs multiple signaling pathways, including autophagy, oxidative stress, inflammation, and translation, suggesting a multifaceted role of ATF4 in the progression of various pathologies. However, ATF4 has been shown to trigger both pro-survival and pro-death pathways, and this, perhaps, can explain the contradictory opinions in current literature regarding targeting ATF4 for clinical application. In this review, we summarized recent published studies from our labs and others that focus on the therapeutic potential of the strategy controlling ATF4 expression in different retinal and neurodegenerative disorders.http://journal.frontiersin.org/article/10.3389/fncel.2017.00410/fullactivating transcription factor 4ER stress responseunfolded protein response (UPR)neurodegenerative diseasesretinal diseasesneurons |
| spellingShingle | Priyamvada M. Pitale Oleg Gorbatyuk Oleg Gorbatyuk Marina Gorbatyuk Neurodegeneration: Keeping ATF4 on a Tight Leash Frontiers in Cellular Neuroscience activating transcription factor 4 ER stress response unfolded protein response (UPR) neurodegenerative diseases retinal diseases neurons |
| title | Neurodegeneration: Keeping ATF4 on a Tight Leash |
| title_full | Neurodegeneration: Keeping ATF4 on a Tight Leash |
| title_fullStr | Neurodegeneration: Keeping ATF4 on a Tight Leash |
| title_full_unstemmed | Neurodegeneration: Keeping ATF4 on a Tight Leash |
| title_short | Neurodegeneration: Keeping ATF4 on a Tight Leash |
| title_sort | neurodegeneration keeping atf4 on a tight leash |
| topic | activating transcription factor 4 ER stress response unfolded protein response (UPR) neurodegenerative diseases retinal diseases neurons |
| url | http://journal.frontiersin.org/article/10.3389/fncel.2017.00410/full |
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