Evidence map›Paper›PMID 40258948›Full record

ArticleScientific reports2025

Uncovering mechanism of hepatotoxicity diseases caused by tetrahydrocannabinol based on novel network toxicology and experimental verification.

Tiantian Zou, Ruilin Zhang, Liping Hu, Genmeng Yang, Xuanyu Chen, Mengqing Wang, Tiantian Cheng, Shengjie Nie, Linlin Liu, Shijun Hong

Abstract read
In one paragraph

Article in Scientific reports, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

10 authors.

Tiantian Zou *NHC Key Laboratory of Drug Addiction Medicine, Kunming Medical University, Kunming, Yunnan Province, China.
Ruilin Zhang *NHC Key Laboratory of Drug Addiction Medicine, Kunming Medical University, Kunming, Yunnan Province, China.
Liping Hu *School of Forensic Medicine, Kunming Medical University, Kunming, Yunnan Province, China.
Genmeng YangNHC Key Laboratory of Drug Addiction Medicine, Kunming Medical University, Kunming, Yunnan Province, China.
Xuanyu ChenSchool of Forensic Medicine, Kunming Medical University, Kunming, Yunnan Province, China.
Mengqing WangSchool of Forensic Medicine, Kunming Medical University, Kunming, Yunnan Province, China.
Tiantian ChengSchool of Forensic Medicine, Kunming Medical University, Kunming, Yunnan Province, China.
Shengjie NieSchool of Forensic Medicine, Kunming Medical University, Kunming, Yunnan Province, China. nieshengjie@126.com.
Linlin LiuNHC Key Laboratory of Drug Addiction Medicine, Kunming Medical University, Kunming, Yunnan Province, China. liull0818@126.com.
Shijun HongNHC Key Laboratory of Drug Addiction Medicine, Kunming Medical University, Kunming, Yunnan Province, China. kmhongshijun@126.com.

Funding

Kunming Medical University Talent Introduction Research Project K132310511 and K132310529Natural Science Foundation of Yunnan Province 202303AC100021the National Natural Science Foundation of China 82260654The NHC Key Lab of Drug Addiction Medicine (Kunming Medical University) Open Projects Fund KN202411 and KN202420
6 · The paper itself

Abstract

This study systematically investigated the molecular mechanisms underlying tetrahydrocannabinol (THC)-induced hepatotoxicity in humans through an integrated approach combining network toxicology, molecular docking, and experimental validation. Our analysis identified 22 core targets associated with THC-mediated hepatotoxicity. Protein-protein interaction (PPI) network analysis revealed significant functional associations among these 22 potential target proteins. KEGG pathway and GO term analyses demonstrated that THC potentially exerts hepatotoxic effects through multiple biological processes, including endocrine resistance, bile secretion, negative regulation of apoptosis, and cellular oxidant detoxification. Disease enrichment analysis further identified several pathological conditions closely associated with THC-induced hepatic damage. Molecular docking simulations demonstrated strong binding affinities between THC and functional domains of 17 target proteins that participated in the aforementioned enriched pathways. An in vitro model of THC-induced hepatocyte injury was successfully established and subsequently validated through RT-qPCR experiment. THC exposure significantly altered the expression patterns of 10 critical target genes: ERBB2, GPX1, MAPK14, NR1H4, SOD1, CXCR2, PPARG, EGFR, TYMS and KDR. The hepatotoxic effects of THC appear to arise from the synergistic interplay of multiple pathways and the coordinated dysfunction of various gene products. These findings elucidate key molecular pathways and therapeutic targets associated with THC-induced hepatotoxicity, providing a theoretical foundation for developing clinical interventions and hepatoprotective strategies against cannabis-related liver damage.

Indexed as

Chemical and Drug Induced Liver InjuryDronabinolHepatocytesHumansLiverMolecular Docking SimulationProtein Interaction MapsDronabinolHepatotoxicityMolecular dockingNetwork toxicologyTetrahydrocannabinolTherapeutic targets

Identifiers

PMID40258948
PMCPMC12012079

What OpenQuestion 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 OpenQuestion graph.