Evidence map›Paper›PMID 30677238›Full record

ArticleCNS neuroscience & therapeutics2019

Endoplasmic reticulum stress induces apoptosis of arginine vasopressin neurons in central diabetes insipidus via PI3K/Akt pathway.

Ming-Feng Zhou, Zhan-Peng Feng, Yi-Chao Ou, Jun-Jie Peng, Kai Li, Hao-Dong Gong, Bing-Hui Qiu, Ya-Wei Liu, Yong-Jia Wang, Song-Tao Qi

Open access · goldAbstract read
In one paragraph

Article in CNS neuroscience & therapeutics, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
1.9field-weighted citation impact, top 14% 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

14 citing papers in PubMed, 20 citations in OpenAlex.

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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

10 authors at 2 institutions in 1 country.

Ming-Feng ZhouDepartment of Neurosurgery, Nanfang Hospital, Southern Medical University, Guangzhou, China.
Zhan-Peng FengDepartment of Neurosurgery, Nanfang Hospital, Southern Medical University, Guangzhou, China.
Yi-Chao OuDepartment of Neurosurgery, Nanfang Hospital, Southern Medical University, Guangzhou, China.
Jun-Jie PengDepartment of Neurosurgery, Nanfang Hospital, Southern Medical University, Guangzhou, China.
Kai LiThe First School of Clinical Medicine, Southern Medical University, Guangzhou, China.
Hao-Dong GongThe First School of Clinical Medicine, Southern Medical University, Guangzhou, China.
Bing-Hui QiuDepartment of Neurosurgery, Nanfang Hospital, Southern Medical University, Guangzhou, China.
Ya-Wei LiuDepartment of Neurosurgery, Nanfang Hospital, Southern Medical University, Guangzhou, China.
Yong-Jia WangThe First School of Clinical Medicine, Southern Medical University, Guangzhou, China.
Song-Tao QiDepartment of Neurosurgery, Nanfang Hospital, Southern Medical University, Guangzhou, China.ORCID 0000-0001-8836-7277
Nanfang Hospital · CNSouthern Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

aimsCentral diabetes insipidus (CDI), a typical complication caused by pituitary stalk injury, often occurs after surgery, trauma, or tumor compression around hypothalamic structures such as the pituitary stalk and optic chiasma. CDI is linked to decreased arginine vasopressin (AVP) neurons in the hypothalamic supraoptic nucleus and paraventricular nucleus, along with a deficit in circulating AVP and oxytocin. However, little has been elucidated about the changes in AVP neurons in CDI. Hence, our study was designed to understand the role of several pathophysiologic changes such as endoplasmic reticulum (ER) stress and apoptosis of AVP neurons in CDI.

methodsIn a novel pituitary stalk electric lesion (PEL) model to mimic CDI, immunofluorescence and immunoblotting were used to understand the underlying regulatory mechanisms.

resultsWe reported that in CDI condition, generated by PEL, ER stress induced apoptosis of AVP neurons via activation of the PI3K/Akt and ERK pathways. Furthermore, application of N-acetylcysteine protected hypothalamic AVP neurons from ER stress-induced apoptosis through blocking the PI3K/Akt and ERK pathways.

conclusionOur findings showed that AVP neurons underwent apoptosis induced by ER stress, and ER stress might play a vital role in CDI condition through the PI3K/Akt and ERK pathways.

Indexed as

AcetylcysteineAnimalsApoptosisArginine VasopressinDiabetes Insipidus, NeurogenicDisease Models, AnimalEndoplasmic Reticulum StressHypothalamusMaleMAP Kinase Signaling SystemNeuronsNeuroprotective AgentsPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktRandom AllocationRats, Sprague-DawleyAcetylcysteineArginine VasopressinNeuroprotective AgentsPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktapoptosiscentral diabetes insipiduscentral nervous systemdrug targetPI3K/Akt pathway

Identifiers

PMID30677238
PMCPMC6488892
OpenAlexW2914263487

What OpenQuestion holds

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LicenceCC BY
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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.