Evidence mapPaperPMID 41796161Full record

ArticleScientific reports2026

Network toxicology study and key target validation of chlorpyrifos-induced nonalcoholic fatty liver disease.

Yapeng Li, Zhengwei Zhang, Hongji Li, Guixin Zhang, Junting Ren, Manyu Gong, Haodong Li, Shibo Sun, Ying Zhang, Na Li and 1 more

Abstract read
In one paragraph

Article in Scientific reports, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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0citing papers in PubMed
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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

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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

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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

11 authors.

Yapeng Li *The Second Affiliated Hospital of Harbin Medical University, Harbin, 150081, China.
Zhengwei Zhang *The Second Affiliated Hospital of Harbin Medical University, Harbin, 150081, China.
Hongji Li *The Second Affiliated Hospital of Harbin Medical University, Harbin, 150081, China.
Guixin Zhang *Qingdao Cardiovascular Hospital, Qingdao, 266000, China.
Junting RenDepartment of Pharmacology (National Key Laboratory of Frigid Zone Cardiovascular Diseases, the State-Province Key Laboratories of Biomedicine-Pharmaceutics of China, Key Laboratory of Cardiovascular Research, Ministry of Education), College of Pharmacy, Harbin Medical University, Harbin, 150081, China.
Manyu GongDepartment of Pharmacology (National Key Laboratory of Frigid Zone Cardiovascular Diseases, the State-Province Key Laboratories of Biomedicine-Pharmaceutics of China, Key Laboratory of Cardiovascular Research, Ministry of Education), College of Pharmacy, Harbin Medical University, Harbin, 150081, China.
Haodong LiDepartment of Pharmacology (National Key Laboratory of Frigid Zone Cardiovascular Diseases, the State-Province Key Laboratories of Biomedicine-Pharmaceutics of China, Key Laboratory of Cardiovascular Research, Ministry of Education), College of Pharmacy, Harbin Medical University, Harbin, 150081, China.
Shibo SunThe Second Affiliated Hospital of Harbin Medical University, Harbin, 150081, China. shibosun8@hrbmu.edu.cn.
Ying ZhangDepartment of Pharmacology (National Key Laboratory of Frigid Zone Cardiovascular Diseases, the State-Province Key Laboratories of Biomedicine-Pharmaceutics of China, Key Laboratory of Cardiovascular Research, Ministry of Education), College of Pharmacy, Harbin Medical University, Harbin, 150081, China. 101153@hrbmu.edu.cn.
Na LiPublic Health Institute of Harbin Medical University, Harbin, 150081, China. 490235647@qq.com.
Xiaoning ChenThe Second Affiliated Hospital of Harbin Medical University, Harbin, 150081, China. wfqcxn@hrbmu.edu.cn.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Chlorpyrifos (CPF) is a widely used insecticide known for its extended persistence in soil and water. It can induce non-alcoholic fatty liver disease (NAFLD) in mice. However, the specific molecular mechanisms responsible for CPF-induced NAFLD remain partially understood. Utilizing network toxicology analysis, we have identified TP53, HSP90AA1, AKT1, and JUN as pivotal driver genes orchestrating NAFLD progression triggered by CPF. A predictive nomogram constructed on these core genes demonstrates promising translational prospects for NAFLD. Gene-set enrichment analysis (GSEA) underscores the significance of the tricarboxylic acid (TCA) cycle and histidine metabolism as critical pathways associated with CPF-induced NAFLD. Evaluation of immune infiltration patterns reveals notable changes in the immunological milieu and accelerated disease advancement in CPF-induced NAFLD. Molecular docking and dynamic simulations provide support for the formation of stable complexes between CPF and proteins encoded by the identified core genes. Ultimately, biomedical experiments confirmed that CPF exacerbates the pathological progression of NAFLD by stabilizing HSP90AA1 protein and promoting the phosphorylation of TP53 and JUN. This study elucidates the molecular mechanisms underpinning CPF-induced NAFLD, providing a theoretical foundation for comprehending its pathogenesis.

Indexed as

ChlorpyrifosInsecticidesNon-alcoholic Fatty Liver DiseaseAnimalsHSP90 Heat-Shock ProteinsLiverMaleMiceMolecular Docking SimulationMolecular Dynamics SimulationTumor Suppressor Protein p53ChlorpyrifosHSP90 Heat-Shock ProteinsInsecticidesTumor Suppressor Protein p53ChlorpyrifosMolecular dockingMolecular dynamics simulationNetwork toxicologyNon-alcoholic fatty liver disease

Identifiers

PMID41796161
PMCPMC13087151

What Socratic holds

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LicenceCC BY-NC-ND
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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 Socratic graph.