Evidence map›Paper›PMID 29181619›Full record

ArticleEndocrine2018

MicroRNA-326 contributes to autoimmune thyroiditis by targeting the Ets-1 protein.

Na Zhao, Hongjin Zou, Jing Qin, Chenling Fan, Yongping Liu, Shuo Wang, Zhongyan Shan, Weiping Teng, Yushu Li

Abstract read
PubMed Publisher
In one paragraph

Article in Endocrine, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
0.6field-weighted citation impact, top 34% 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

8 citing papers in PubMed, 17 citations in OpenAlex.

  1. Review
  2. Single-Cell RNA Sequencing of Thyroid Tissues Reveals Pathogenesis of Graves' Disease.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026
    Article
  3. Article
  4. Article
  5. Article
  6. A Review of miR-326 and Female Related Diseases.Acta histochemica et cytochemica · 2021
    Review
  7. Review
  8. Frontiers in immunology · 2021
    Article
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

9 authors at 2 institutions in 1 country.

Na ZhaoDepartment of Endocrinology and Metabolism, Institute of Endocrinology, Liaoning Provincial Key Laboratory of Endocrine Diseases, The First Affiliated Hospital of China Medical University, Shenyang, 110001, PR China.
Hongjin ZouDepartment of Endocrinology and Metabolism, Institute of Endocrinology, Liaoning Provincial Key Laboratory of Endocrine Diseases, The First Affiliated Hospital of China Medical University, Shenyang, 110001, PR China.
Jing QinDepartment of Endocrinology and Metabolism, Institute of Endocrinology, Liaoning Provincial Key Laboratory of Endocrine Diseases, The First Affiliated Hospital of China Medical University, Shenyang, 110001, PR China.
Chenling FanDepartment of Endocrinology and Metabolism, Institute of Endocrinology, Liaoning Provincial Key Laboratory of Endocrine Diseases, The First Affiliated Hospital of China Medical University, Shenyang, 110001, PR China.
Yongping LiuDepartment of Endocrinology and Metabolism, Institute of Endocrinology, Liaoning Provincial Key Laboratory of Endocrine Diseases, The First Affiliated Hospital of China Medical University, Shenyang, 110001, PR China.
Shuo WangDepartment of Endocrinology and Metabolism, Institute of Endocrinology, Liaoning Provincial Key Laboratory of Endocrine Diseases, The First Affiliated Hospital of China Medical University, Shenyang, 110001, PR China.
Zhongyan ShanDepartment of Endocrinology and Metabolism, Institute of Endocrinology, Liaoning Provincial Key Laboratory of Endocrine Diseases, The First Affiliated Hospital of China Medical University, Shenyang, 110001, PR China.
Weiping TengDepartment of Endocrinology and Metabolism, Institute of Endocrinology, Liaoning Provincial Key Laboratory of Endocrine Diseases, The First Affiliated Hospital of China Medical University, Shenyang, 110001, PR China.
Yushu LiDepartment of Endocrinology and Metabolism, Institute of Endocrinology, Liaoning Provincial Key Laboratory of Endocrine Diseases, The First Affiliated Hospital of China Medical University, Shenyang, 110001, PR China. liyushu@hotmail.com.
China Medical University · CNFirst Hospital of China Medical University · CN

Funding

Chinese National Natural Science Foundation 81471003
6 · The paper itself

Abstract

purposeMicroRNA-326 (miR-326), as a member of the microRNA (miRNA) family, which includes endogenous single-stranded, conserved, noncoding small RNAs, has been reported to play important roles in autoimmune diseases such as multiple sclerosis and systemic lupus erythematosus. However, few studies of the role of miR-326 in autoimmune thyroiditis (AIT) have been published. Here, we explored the roles of miR-326 and the involved pathway in iodine-induced AIT.

methodsNOD.H-2

resultsIn this study, we found that Th17 cells were significantly increased with a high expression of miR-326 in an iodine-induced thyroiditis NOD.H-2

conclusionsThe results of our study suggest that miR-326 may target the Ets-1 protein to contribute to iodide-induced thyroiditis, providing a new theoretical basis for the use of miRNA targeting therapy for the treatment of autoimmune diseases.

Indexed as

AnimalsDisease Models, AnimalFemaleGene Expression RegulationIodineMiceMice, Inbred NODMice, TransgenicMicroRNAsProto-Oncogene Protein c-ets-1Th17 CellsThyroiditis, AutoimmuneT-Lymphocytes, RegulatoryEts1 protein, mouseIodineMicroRNAsMIRN326 microRNA, mouseProto-Oncogene Protein c-ets-1Autoimmune diseasesEts-1MicroRNA-326Th17Thyroiditis

Identifiers

PMID29181619
OpenAlexW2770524708

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.