Evidence map›Paper›PMID 42343984›Full record

ArticleInternational journal of endocrinology2026

Deletion of miR-122-5p Exacerbated Hyperthyroidism-Induced Liver Injury by Regulating Ferroptosis.

Guoxian Zhu, Lidan Zhang, Wenbao Huang, Jiexia Ding, Lifei Yu, Xiangfei Xu

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in International journal of endocrinology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing 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

1 citing paper in PubMed.

  1. 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

6 authors.

Guoxian ZhuDepartment of Infectious Diseases, School of Medicine, Affiliated Hangzhou First People's Hospital, Westlake University, Hangzhou, Zhejiang, China, westlake.edu.cn.ORCID https://orcid.org/0009-0001-5196-9802
Lidan ZhangDepartment of Infectious Diseases, School of Medicine, Affiliated Hangzhou First People's Hospital, Westlake University, Hangzhou, Zhejiang, China, westlake.edu.cn.
Wenbao HuangDepartment of Infectious Diseases, School of Medicine, Affiliated Hangzhou First People's Hospital, Westlake University, Hangzhou, Zhejiang, China, westlake.edu.cn.
Jiexia DingDepartment of Infectious Diseases, School of Medicine, Affiliated Hangzhou First People's Hospital, Westlake University, Hangzhou, Zhejiang, China, westlake.edu.cn.
Lifei YuDepartment of Infectious Diseases, School of Medicine, Affiliated Hangzhou First People's Hospital, Westlake University, Hangzhou, Zhejiang, China, westlake.edu.cn.
Xiangfei XuDepartment of Infectious Diseases, School of Medicine, Affiliated Hangzhou First People's Hospital, Westlake University, Hangzhou, Zhejiang, China, westlake.edu.cn.ORCID https://orcid.org/0009-0000-1003-5969

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The aim of this study was to evaluate the effect and mechanism of miR-122-5p on hepatic injury induced by hyperthyroidism. Male Sprague Dawley rats were divided into three groups: a normal thyroid function group (sham), a levothyroxine (LT4)-induced hyperthyroidism group (T4 sodium), and a hyperthyroidism group treated with a miR-122-5p inhibitor (T4 sodium + antagomir-122-5p). Liver tissue pathology, ferroptosis and inflammatory markers, and miR-122-5p expression were assessed. Finally, rat hepatocytes (BRL-3A) were treated with carbon tetrachloride (CCL4) to explore the role of the miR-122-5p/CCDC6 axis in hepatocyte injury. We found that miR-122-5p was expressed at low levels in liver tissues from hyperthyroid rats. Inhibition of miR-122-5p aggravated liver tissue injury. Additionally, in hyperthyroid rats, inflammatory factors, iron content, and markers of ferroptosis were upregulated by miR-122-5p inhibitors. Mechanistically, miR-122-5p was found to bind to CCDC6 and negatively regulate CCDC6 expression. Furthermore, miR-122-5p deletion induced hepatocyte injury by exacerbating the ferroptosis process and mitochondrial damage in CCL4-treated hepatocytes, a process dependent on CCDC6 expression. The miR-122-5p/CCDC6 axis plays a protective role in hyperthyroidism-induced liver injury and serves as a potential target for the clinical treatment of hyperthyroidism-associated liver disease.

Indexed as

CCDC6ferroptosishyperthyroidismliver damagemiR-122-5p

Identifiers

PMID42343984
PMCPMC13287836

What OpenQuestion holds

Textmetadata
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.