Evidence map›Paper›PMID 40687582›Full record

ArticleFrontiers in endocrinology2025

Involvement of miR-205-5p in mediating the development of nodular thyroid disease associated with coal worker's pneumoconiosis via pulmonary extracellular vesicles.

Feng Zhao, Yu Hao, Hongzhen Zhang

Abstract read
In one paragraph

Article in Frontiers in endocrinology, 2025. 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

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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

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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. Review
4 · The record

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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

3 authors.

Feng ZhaoThyroid and Breast Surgery Department, The First Hospital of Anhui University of Science and Technology, Huainan First People's Hospital, Huainan, China.
Yu Hao *Breast Surgery, Provincial Hospital of Weihai City, Weihai, Shandong, China.
Hongzhen ZhangSchool of Public Health, Anhui University of Science and Technology, Huainan, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Objective: Coal worker's pneumoconiosis (CWP) is an occupational disease, and the mechanisms underlying the development of its complication, nodular thyroid disease (NTD), remain unclear. This study aimed to investigate the role of miR-205-5p (miR-205-5p) in the development of nodular thyroid disease associated with coal worker's pneumoconiosis. Methods: The potential role of pulmonary extracellular vesicles in triggering coal worker's pneumoconiosis-associated nodular thyroid disease was explored. RNA was extracted from isolated extracellular vesicle samples, and real-time fluorescent quantitative RT-qPCR was performed using specific primers and probes. The levels of miR-205-5p in the extracellular vesicles from the supernatant of each treatment group were compared, and the significant expression of miR-205-5p in the extracellular vesicles was detected by RT-qPCR to evaluate the regulatory role of lung-derived extracellular vesicles in the development of coal worker's pneumoconiosis-associated nodular thyroid disease. In addition, cell proliferation, apoptosis, and invasion capabilities were assessed using the CCK-8 assay for cell proliferation activity, Annexin V-FITC/PI double staining and flow cytometry for cell apoptosis rate, and Transwell assay for cell invasion ability. Results: By isolating, purifying, and analyzing extracellular vesicles from coal worker's pneumoconiosis patients and healthy controls, it was found that the expression of miR-205-5p in the plasma of coal worker's pneumoconiosis patients was significantly higher than that in the healthy controls ( Conclusion: miR-205-5p in pulmonary extracellular vesicles mediates the development of nodular thyroid disease associated with coal worker's pneumoconiosis through the ATF4/CHOP signaling axis. Further research is essential to comprehensively investigate the specific targets through which miR-205-5p derived from pulmonary extracellular vesicles triggers the development of nodular thyroid disease associated with coal worker's pneumoconiosis via the ATF4/CHOP signaling axis.

Indexed as

AnthracosisExtracellular VesiclesLungMicroRNAsApoptosisCase-Control StudiesCell ProliferationHumansMaleMiddle AgedTranscription Factor CHOPDDIT3 protein, humanMicroRNAsMIR205, humanTranscription Factor CHOPATF4/CHOP signaling axiscoal worker’s pneumoconiosisMiR-205-5pnodular thyroid diseasepulmonary extracellular vesicles

Identifiers

PMID40687582
PMCPMC12271885

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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.