Evidence map›Paper›PMID 41490975›Full record

ArticleNPJ science of food2026

Application of HepG2-derived organoid and organ-on-a-chip platforms in elucidating selenium-mediated protection against cadmium-induced liver dysfunction.

Meng Ren, Qing Feng, Surui Lu, Wen Xiao, Qihong Deng, Xiaoyan Yang, Cheng Yan, Zhanhong Ren, Biao Yan, Yang Wu and 4 more

Abstract read
In one paragraph

Article in NPJ science of food, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing 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

2 citing papers in PubMed.

  1. Article
  2. Artificial Intelligence Across the Drug Development Lifecycle.Medical sciences (Basel, Switzerland) · 2026
    Review
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

14 authors.

Meng RenHubei Key Laboratory of Environmental Risks and Related Diseases Precision Control, Hubei University of Science and Technology, Xianning, China.
Qing FengHubei Key Laboratory of Environmental Risks and Related Diseases Precision Control, Hubei University of Science and Technology, Xianning, China.
Surui LuHubei Key Laboratory of Environmental Risks and Related Diseases Precision Control, Hubei University of Science and Technology, Xianning, China.
Wen XiaoInstitute of Eastern-Himalaya Biodiversity Research, Dali University, Dali, Yunnan, China.
Qihong DengSchool of Public Health, Zhengzhou University, Zhengzhou, China.
Xiaoyan YangInstitute of Eastern-Himalaya Biodiversity Research, Dali University, Dali, Yunnan, China.
Cheng YanSchool of Environmental Studies, China University of Geosciences (Wuhan), Wuhan, China.
Zhanhong RenHubei Key Laboratory of Environmental Risks and Related Diseases Precision Control, Hubei University of Science and Technology, Xianning, China.
Biao YanHubei Key Laboratory of Environmental Risks and Related Diseases Precision Control, Hubei University of Science and Technology, Xianning, China.
Yang WuHubei Key Laboratory of Environmental Risks and Related Diseases Precision Control, Hubei University of Science and Technology, Xianning, China.
Shaodan HuangDepartment of Occupational and Environmental Health Sciences, School of Public Health, Peking University, Beijing, China.
Xu YangHubei Key Laboratory of Environmental Risks and Related Diseases Precision Control, Hubei University of Science and Technology, Xianning, China.
Ping MaHubei Key Laboratory of Environmental Risks and Related Diseases Precision Control, Hubei University of Science and Technology, Xianning, China. mping68@126.com.
Liqin SuNational Institute of Environmental Health, Chinese Center for Disease Control and Prevention, Beijing, China. suliqin@nieh.chinacdc.cn.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

HepG2 cells were cultured into liver organoids (more native liver-like than 2D cultures) and integrated into a microfluidic chip, which regulates flow, nutrients, and waste to simulate in vivo hepatic microcirculation. Key findings: Cadmium (Cd) exposure shows a positive dose-response with liver damage; 40 ng/mL selenium (Se) alleviates 3 sets of liver biochemical dysfunctions under 40 μg/mL Cd co-exposure, but 160/640 ng/mL Se diminishes this protection. Metabolomics (40 μg/mL Cd vs. 640 ng/mL Se+Cd) identified two mechanisms: high Se induces oxidative stress and disrupts liver cellular metabolism. This study provides data/theory for rational Se use against Cd-induced liver dysfunction. The platform integrates organoid/organ-on-a-chip assessments with microfluidic metabolomics (a cross-scale toxicological system) and informs 3D cell model development.

Identifiers

PMID41490975
PMCPMC12827379

What Socratic holds

Textmetadata
LicenceCC BY-NC-ND
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 Socratic graph.