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The ER stress-autophagy axis: implications for cognitive dysfunction in diabetes mellitus
Unfolded protein response (UPR) often coordinates with autophagy to maintain cellular proteostasis. Disturbance of proteostasis correlates with diseases including diabetes and neurological complications. In a recent article in Clinical Science, Kong et al. highlighted the critical role of endoplasmi...
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Portland Press Ltd.
2020
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7276635/ https://www.ncbi.nlm.nih.gov/pubmed/32501495 http://dx.doi.org/10.1042/CS20200235 |
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author | Zhu, Qingzhang |
author_facet | Zhu, Qingzhang |
author_sort | Zhu, Qingzhang |
collection | PubMed |
description | Unfolded protein response (UPR) often coordinates with autophagy to maintain cellular proteostasis. Disturbance of proteostasis correlates with diseases including diabetes and neurological complications. In a recent article in Clinical Science, Kong et al. highlighted the critical role of endoplasmic reticulum (ER) stress-autophagy axis in maintaining cognitive functions and provided pharmacological evidence with respect to cognitive improvements in a diabetic mouse model. These novel findings present new insights into the pathological mechanisms and therapeutic implications with the ER stress modulators in diabetes-related cognitive dysfunction. |
format | Online Article Text |
id | pubmed-7276635 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2020 |
publisher | Portland Press Ltd. |
record_format | MEDLINE/PubMed |
spelling | pubmed-72766352020-06-16 The ER stress-autophagy axis: implications for cognitive dysfunction in diabetes mellitus Zhu, Qingzhang Clin Sci (Lond) Diabetes & Metabolic Disorders Unfolded protein response (UPR) often coordinates with autophagy to maintain cellular proteostasis. Disturbance of proteostasis correlates with diseases including diabetes and neurological complications. In a recent article in Clinical Science, Kong et al. highlighted the critical role of endoplasmic reticulum (ER) stress-autophagy axis in maintaining cognitive functions and provided pharmacological evidence with respect to cognitive improvements in a diabetic mouse model. These novel findings present new insights into the pathological mechanisms and therapeutic implications with the ER stress modulators in diabetes-related cognitive dysfunction. Portland Press Ltd. 2020-06 2020-06-05 /pmc/articles/PMC7276635/ /pubmed/32501495 http://dx.doi.org/10.1042/CS20200235 Text en © 2020 The Author(s). https://creativecommons.org/licenses/by-nc-nd/4.0/ This is an open access article published by Portland Press Limited on behalf of the Biochemical Society and distributed under the Creative Commons Attribution License 4.0 (CC BY-NC-ND). Open access for this article was enabled by the participation of University of Texas Southwestern Medical Centre in an all-inclusive Read & Publish pilot with Portland Press and the Biochemical Society under a transformative agreement with EBSCO. |
spellingShingle | Diabetes & Metabolic Disorders Zhu, Qingzhang The ER stress-autophagy axis: implications for cognitive dysfunction in diabetes mellitus |
title | The ER stress-autophagy axis: implications for cognitive dysfunction in diabetes mellitus |
title_full | The ER stress-autophagy axis: implications for cognitive dysfunction in diabetes mellitus |
title_fullStr | The ER stress-autophagy axis: implications for cognitive dysfunction in diabetes mellitus |
title_full_unstemmed | The ER stress-autophagy axis: implications for cognitive dysfunction in diabetes mellitus |
title_short | The ER stress-autophagy axis: implications for cognitive dysfunction in diabetes mellitus |
title_sort | er stress-autophagy axis: implications for cognitive dysfunction in diabetes mellitus |
topic | Diabetes & Metabolic Disorders |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7276635/ https://www.ncbi.nlm.nih.gov/pubmed/32501495 http://dx.doi.org/10.1042/CS20200235 |
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