Evidence map›Paper›PMID 27793043›Full record

ArticleOncotarget2016

Endoplasmic reticulum stress-induced neuronal inflammatory response and apoptosis likely plays a key role in the development of diabetic encephalopathy.

Zhouguang Wang, Yan Huang, Yi Cheng, Yi Tan, Fenzan Wu, Jiamin Wu, Hongxue Shi, Hongyu Zhang, Xichong Yu, Hongchang Gao and 6 more

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers.

0numbers the graph read from it
0cells of the map it votes in
42citing papers in PubMed
4.2field-weighted citation impact, top 6% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

42 citing papers in PubMed, 82 citations in OpenAlex.

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  9. FoliumPharmaceutical biology · 2022
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

16 authors at 2 institutions in 2 countries.

Zhouguang WangChinese-American Research Institute for Diabetic Complications, School of Pharmaceutical Science, Key Laboratory of Biotechnology and Pharmaceutical Engineering, Wenzhou Medical University, Wenzhou, Zhejiang, China.
Yan HuangChinese-American Research Institute for Diabetic Complications, School of Pharmaceutical Science, Key Laboratory of Biotechnology and Pharmaceutical Engineering, Wenzhou Medical University, Wenzhou, Zhejiang, China.
Yi ChengChinese-American Research Institute for Diabetic Complications, School of Pharmaceutical Science, Key Laboratory of Biotechnology and Pharmaceutical Engineering, Wenzhou Medical University, Wenzhou, Zhejiang, China.
Yi TanChinese-American Research Institute for Diabetic Complications, School of Pharmaceutical Science, Key Laboratory of Biotechnology and Pharmaceutical Engineering, Wenzhou Medical University, Wenzhou, Zhejiang, China.
Fenzan WuChinese-American Research Institute for Diabetic Complications, School of Pharmaceutical Science, Key Laboratory of Biotechnology and Pharmaceutical Engineering, Wenzhou Medical University, Wenzhou, Zhejiang, China.
Jiamin WuChinese-American Research Institute for Diabetic Complications, School of Pharmaceutical Science, Key Laboratory of Biotechnology and Pharmaceutical Engineering, Wenzhou Medical University, Wenzhou, Zhejiang, China.
Hongxue ShiChinese-American Research Institute for Diabetic Complications, School of Pharmaceutical Science, Key Laboratory of Biotechnology and Pharmaceutical Engineering, Wenzhou Medical University, Wenzhou, Zhejiang, China.
Hongyu ZhangChinese-American Research Institute for Diabetic Complications, School of Pharmaceutical Science, Key Laboratory of Biotechnology and Pharmaceutical Engineering, Wenzhou Medical University, Wenzhou, Zhejiang, China.
Xichong YuChinese-American Research Institute for Diabetic Complications, School of Pharmaceutical Science, Key Laboratory of Biotechnology and Pharmaceutical Engineering, Wenzhou Medical University, Wenzhou, Zhejiang, China.
Hongchang GaoChinese-American Research Institute for Diabetic Complications, School of Pharmaceutical Science, Key Laboratory of Biotechnology and Pharmaceutical Engineering, Wenzhou Medical University, Wenzhou, Zhejiang, China.
Li LinChinese-American Research Institute for Diabetic Complications, School of Pharmaceutical Science, Key Laboratory of Biotechnology and Pharmaceutical Engineering, Wenzhou Medical University, Wenzhou, Zhejiang, China.
Jun CaiDepartment of Pediatrics, Children's Hospital Research Institute, the University of Louisville, Louisville, Kentucky, USA.
Jinsan ZhangChinese-American Research Institute for Diabetic Complications, School of Pharmaceutical Science, Key Laboratory of Biotechnology and Pharmaceutical Engineering, Wenzhou Medical University, Wenzhou, Zhejiang, China.
Xiaokun LiChinese-American Research Institute for Diabetic Complications, School of Pharmaceutical Science, Key Laboratory of Biotechnology and Pharmaceutical Engineering, Wenzhou Medical University, Wenzhou, Zhejiang, China.
Lu CaiChinese-American Research Institute for Diabetic Complications, School of Pharmaceutical Science, Key Laboratory of Biotechnology and Pharmaceutical Engineering, Wenzhou Medical University, Wenzhou, Zhejiang, China.
Jian XiaoChinese-American Research Institute for Diabetic Complications, School of Pharmaceutical Science, Key Laboratory of Biotechnology and Pharmaceutical Engineering, Wenzhou Medical University, Wenzhou, Zhejiang, China.
Wenzhou Medical University · CNUniversity of Louisville Hospital · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

We assumed that diabetic encephalopathy (DEP) may be induced by endoplasmic reticulum (ER)-mediated inflammation and apoptosis in central nervous system. To test this notion, here we investigated the neuronal ER stress and associated inflammation and apoptosis in a type 2 diabetes model induced with high-fat diet/streptozotocin in Sprague-Dawley rats. Elevated expressions of ER stress markers, including glucose-regulated protein 78 (GRP78), activating transcription factor-6 (ATF-6), X-box binding protein-1 (XBP-1), and C/EBP homologous protein, and phosphor-Jun N-terminal kinase (p-JNK) were evident in the hippocampus CA1 of diabetic rats. These changes were also accompanied with the activation of NF-κB and the increased levels of inflammatory cytokines, tumor necrosis factor-α (TNF-α) and Interleukin-6 (IL-6). Mechanistic study with in vitro cultured hippocampus neurons exposed to high glucose (HG), which induced a diabetes-like effects, shown by increased ER stress, JNK and NF-κB activation, and inflammatory response. Inhibition of ER stress by 4-phenylbutyrate (4-PBA) or blockade of JNK activity by specific inhibitor or transfection of DN-JNK attenuated HG-induced inflammation and associated apoptosis. To validate the in vitro finding, in vivo application of 4-PBA resulted in a significant reduction of diabetes-induced neuronal ER stress, inflammation and cell death, leading to the prevention of DEP. These results suggest that diabetes-induced neuronal ER stress plays the critical role for diabetes-induced neuronal inflammation and cell death, leading to the development of DEP.

Indexed as

ApoptosisEndoplasmic Reticulum StressActivating Transcription Factor 6AnimalsAnti-Inflammatory AgentsBehavior, AnimalBrain DiseasesCells, CulturedCognitionDiabetes Mellitus, ExperimentalDiabetes Mellitus, Type 2Dose-Response Relationship, DrugEndoplasmic Reticulum Chaperone BiPHeat-Shock ProteinsHippocampusInterleukin-6Activating Transcription Factor 6Anti-Inflammatory AgentsAtf6 protein, ratDdit3 protein, ratEndoplasmic Reticulum Chaperone BiPGRP78 protein, ratHeat-Shock ProteinsInterleukin-6JNK Mitogen-Activated Protein KinasesNF-kappa BProtein Kinase InhibitorsTranscription Factor CHOPTumor Necrosis Factor-alphaX-Box Binding Protein 1Xbp1 protein, ratapoptosisdiabetesER stressinflammationp-JNK

Identifiers

PMID27793043
PMCPMC5346653
OpenAlexW2542776108

What OpenQuestion holds

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LicenceCC BY
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.