Evidence map›Paper›PMID 30610461›Full record

ReviewNeuroscience bulletin2019

Expression and Function of Zinc-α2-Glycoprotein.

Xin Wei, Xi Liu, Changhong Tan, Lijuan Mo, Hui Wang, Xi Peng, Fen Deng, Lifeng Chen

Erratum issuedOpen access · bronzeAbstract readReview
In one paragraph

Review in Neuroscience bulletin, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 43 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
43citing papers in PubMed, 1 pooled it
2.6field-weighted citation impact, top 10% 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

43 citing papers in PubMed, 1 synthesis or guideline pooled it, 60 citations in OpenAlex.

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  6. A potential drug target in epilepsy and its role in other neurological disorders.Naunyn-Schmiedeberg's archives of pharmacology · 2026
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

8 authors at 3 institutions in 1 country.

Xin WeiDepartment of Neurology, The Second Affiliated Hospital of Chongqing Medical University, Chongqing, 400010, China.
Xi LiuDepartment of Neurology, The Second Affiliated Hospital of Chongqing Medical University, Chongqing, 400010, China.
Changhong TanDepartment of Neurology, The Second Affiliated Hospital of Chongqing Medical University, Chongqing, 400010, China.
Lijuan MoDepartment of Neurology, The Second Affiliated Hospital of Chongqing Medical University, Chongqing, 400010, China.
Hui WangDepartment of Neurology, The Second Affiliated Hospital of Chongqing Medical University, Chongqing, 400010, China.
Xi PengDepartment of Neurology, The Second Affiliated Hospital of Chongqing Medical University, Chongqing, 400010, China.
Fen DengDepartment of Neurology, The Second Affiliated Hospital of Chongqing Medical University, Chongqing, 400010, China.
Lifeng ChenDepartment of Neurology, The Second Affiliated Hospital of Chongqing Medical University, Chongqing, 400010, China. lifen_chen@163.com.
Chongqing Medical University · CNDalian Medical University · CNSecond Affiliated Hospital of Chongqing Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Zinc-α2-glycoprotein (ZAG), encoded by the AZGP1 gene, is a major histocompatibility complex I molecule and a lipid-mobilizing factor. ZAG has been demonstrated to promote lipid metabolism and glucose utilization, and to regulate insulin sensitivity. Apart from adipose tissue, skeletal muscle, liver, and kidney, ZAG also occurs in brain tissue, but its distribution in brain is debatable. Only a few studies have investigated ZAG in the brain. It has been found in the brains of patients with Krabbe disease and epilepsy, and in the cerebrospinal fluid of patients with Alzheimer disease, frontotemporal lobe dementia, and amyotrophic lateral sclerosis. Both ZAG protein and AZGP1 mRNA are decreased in epilepsy patients and animal models, while overexpression of ZAG suppresses seizure and epileptic discharges in animal models of epilepsy, but knowledge of the specific mechanism of ZAG in epilepsy is limited. In this review, we summarize the known roles and molecular mechanisms of ZAG in lipid metabolism and glucose metabolism, and in the regulation of insulin sensitivity, and discuss the possible mechanisms by which it suppresses epilepsy.

Indexed as

Insulin ResistanceLipid MetabolismAdipocytesAdipokinesAnimalsBrainCarrier ProteinsEpilepsyGlucoseGlycoproteinsHumansNeuronsSignal TransductionZn-Alpha-2-GlycoproteinAdipokinesAZGP1 protein, humanCarrier ProteinsGlucoseGlycoproteinsZn-Alpha-2-GlycoproteinGlucoseInsulin sensitivityLipidMetabolismNeuronZinc-α2-glycoprotein

Identifiers

PMID30610461
PMCPMC6527650
OpenAlexW2908052005

What OpenQuestion holds

Textmetadata
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.