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. 2020 Jun 12;134(11):1255-1258.
doi: 10.1042/CS20200235.

The ER stress-autophagy axis: implications for cognitive dysfunction in diabetes mellitus

Qingzhang Zhu  1
Affiliations

The ER stress-autophagy axis: implications for cognitive dysfunction in diabetes mellitus

Qingzhang Zhu. Clin Sci (Lond). .

Abstract

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.

Keywords: ER stress; autophagy; cognitive dysfunction; diabetes.

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Conflict of interest statement

The author declares that there are no competing interests associated with manuscript.

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.

Figures

Figure 1
Figure 1. The ER stress-autophagy axis regulates diabetes-related cognitive dysfunction
(A) At normal state, hippocampal neurons survive with low levels of ER stress and autophagy, whereas in diabetes, unresolved ER stress further enhances autophagy and ultimately lead to apoptosis, and thus declines cognitive functions. (B) Cross-talk of ER stress-autophagy axis. Details presented in the text.
See this image and copyright information in PMC

Comment on

  • 10.1042/CS20171432

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