Evidence map›Paper›PMID 27340675›Full record

ArticleJournal of diabetes research2016

Par-4/NF-κB Mediates the Apoptosis of Islet β Cells Induced by Glucolipotoxicity.

Wu QiNan, Gan XiaGuang, Lei XiaoTian, Deng WuQuan, Zhang Ling, Chen Bing

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Journal of diabetes research, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
–field-weighted citation impact
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

13 citing papers in PubMed.

  1. Type 2 Diabetes From the Perspective of Telomere Biology.Endocrinology, diabetes & metabolism · 2026
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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

6 authors.

Wu QiNanEndocrine Department, The First Affiliated Hospital of the Third Military Medical University, Chong Qing 400038, China.
Gan XiaGuangEndocrine Department, The First Affiliated Hospital of the Third Military Medical University, Chong Qing 400038, China.
Lei XiaoTianEndocrine Department, The First Affiliated Hospital of the Third Military Medical University, Chong Qing 400038, China.
Deng WuQuanEndocrine Department, The First Affiliated Hospital of the Third Military Medical University, Chong Qing 400038, China.
Zhang LingOutpatient Department, The First Affiliated Hospital of the Third Military Medical University, Chong Qing 400038, China.
Chen BingEndocrine Department, The First Affiliated Hospital of the Third Military Medical University, Chong Qing 400038, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Apoptosis of islet β cells is a primary pathogenic feature of type 2 diabetes, and ER stress and mitochondrial dysfunction play important roles in this process. Previous research has shown that prostate apoptosis response-4 (Par-4)/NF-κB induces cancer cell apoptosis through endoplasmic reticulum (ER) stress and mitochondrial dysfunction. However, the mechanism by which Par-4/NF-κB induces islet β cell apoptosis remains unknown. We used a high glucose/palmitate intervention to mimic type 2 diabetes in vitro. We demonstrated that the high glucose/palmitate intervention induced the expression and secretion of Par-4. It also causes increased expression and activation of NF-κB, which induced NIT-1 cell apoptosis and dysfunction. Overexpression of Par-4 potentiates these effects, whereas downregulation of Par-4 attenuates them. Inhibition of NF-κB inhibited the Par-4-induced apoptosis. Furthermore, these effects occurred through the ER stress cell membrane and mitochondrial pathway of apoptosis. Our findings reveal a novel role for Par-4/NF-κB in islet β cell apoptosis and type 2 diabetes.

Indexed as

AnimalsApoptosisApoptosis Regulatory ProteinsCell LineDiabetes Mellitus, Type 2Endoplasmic Reticulum StressGlucoseInsulin-Secreting CellsIn Vitro TechniquesMiceMitochondriaNF-kappa BPalmitatesApoptosis Regulatory ProteinsGlucoseNF-kappa BPalmitatesprostate apoptosis response-4 protein

Identifiers

PMID27340675
PMCPMC4906207

What OpenQuestion holds

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Registered trials

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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.