Evidence map›Paper›PMID 29434604›Full record

ArticleFrontiers in immunology2018

Increased Interleukin-23 in Hashimoto's Thyroiditis Disease Induces Autophagy Suppression and Reactive Oxygen Species Accumulation.

Tingting Zheng, Chengcheng Xu, Chaoming Mao, Xiao Mou, Fei Wu, Xuefeng Wang, Ling Bu, Yuepeng Zhou, Xuan Luo, Qingyan Lu and 5 more

Open access · goldAbstract read
In one paragraph

Article in Frontiers in immunology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
1.8field-weighted citation impact, top 15% 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

26 citing papers in PubMed, 48 citations in OpenAlex.

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  16. Orthodontic loading activates cell-specific autophagy in a force-dependent manner.American journal of orthodontics and dentofacial orthopedics : official publication of the American Association of Orthodontists, its constituent societies, and the American Board of Orthodontics · 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

15 authors at 3 institutions in 1 country.

Tingting ZhengDepartment of Nuclear Medicine, The Affiliated Hospital of Jiangsu University, Zhenjiang, China.
Chengcheng XuDepartment of Nuclear Medicine, The Affiliated Hospital of Jiangsu University, Zhenjiang, China.
Chaoming MaoDepartment of Nuclear Medicine, The Affiliated Hospital of Jiangsu University, Zhenjiang, China.
Xiao MouDepartment of Nuclear Medicine, The Affiliated Hospital of Jiangsu University, Zhenjiang, China.
Fei WuDepartment of Nuclear Medicine, The Affiliated Hospital of Jiangsu University, Zhenjiang, China.
Xuefeng WangDepartment of Nuclear Medicine, The Affiliated Hospital of Jiangsu University, Zhenjiang, China.
Ling BuDepartment of Nuclear Medicine, The Affiliated Hospital of Jiangsu University, Zhenjiang, China.
Yuepeng ZhouInstitute of Oncology, The Affiliated Hospital of Jiangsu University, Zhenjiang, China.
Xuan LuoDepartment of Nuclear Medicine, The Affiliated Hospital of Jiangsu University, Zhenjiang, China.
Qingyan LuDepartment of Nuclear Medicine, The Affiliated Hospital of Jiangsu University, Zhenjiang, China.
Hongli LiuDepartment of Nuclear Medicine, The Affiliated Hospital of Jiangsu University, Zhenjiang, China.
Guoyue YuanDepartment of Nuclear Medicine, The Affiliated Hospital of Jiangsu University, Zhenjiang, China.
Shengjun WangDepartment of Laboratory Immunology, Jiangsu University School of Medicine, Zhenjiang, China.
Deyu ChenInstitute of Oncology, The Affiliated Hospital of Jiangsu University, Zhenjiang, China.
Yichuan XiaoDepartment of Nuclear Medicine, The Affiliated Hospital of Jiangsu University, Zhenjiang, China.
Jiangsu University · CNAffiliated Hospital of Jiangsu University · CNShanghai Jiao Tong University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Hashimoto's thyroiditis (HT) represents the most common organ-specific autoimmune disease. Inflammatory factors and reactive oxygen species (ROS) play detrimental roles during the pathogenesis of HT. In this study, we found that thyroid follicular cells (TFCs) from HT patients expressed an elevated level of interleukin-23 (IL-23), which contributed to autophagy suppression and ROS accumulation. Additionally, IL-23-induced autophagy suppression and ROS accumulation in human TFCs was attributed to AKT/mTOR/NF-κB signaling pathway activation. Inhibition of either IL-23 by a specific neutralization antibody, or mTOR by rapamycin, or NF-κB by IKK-16, significantly reversed the autophagy suppression and ROS accumulation. These results demonstrate a key role for IL-23 in HT pathogenesis and provide a potential therapeutic strategy against IL-23 or its signaling pathway in HT.

Indexed as

AutophagyAdultBiomarkersCell LineCytokinesFemaleGene ExpressionHashimoto DiseaseHumansInflammation MediatorsInterleukin-23MaleMiddle AgedNF-kappa BProto-Oncogene Proteins c-aktReactive Oxygen SpeciesBiomarkersCytokinesIL23R protein, humanInflammation MediatorsInterleukin-23NF-kappa BProto-Oncogene Proteins c-aktReactive Oxygen SpeciesReceptors, InterleukinTOR Serine-Threonine KinasesAKT/mTOR/NF-κBautophagyHashimoto’s thyroiditisinterleukin-23reactive oxygen species

Identifiers

PMID29434604
PMCPMC5796905
OpenAlexW2793728542

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.