Evidence map›Paper›PMID 32835833›Full record

ArticleToxicology letters2020

Comprehensive analysis of transcriptomics and metabolomics to understand triptolide-induced liver injury in mice.

Jie Zhao, Cen Xie, Kanglong Wang, Shogo Takahashi, Kristopher W Krausz, Dasheng Lu, Qiong Wang, Yuhong Luo, Xianqiong Gong, Xiyan Mu and 3 more

Open access · greenAbstract read
In one paragraph

Article in Toxicology letters, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
9.7field-weighted citation impact, top 2% of its field
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

25 citing papers in PubMed, 91 citations in OpenAlex.

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  4. The Impact ofAnimals : an open access journal from MDPI · 2025
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  5. Ginkgolic acid inhibits CD8Journal of pharmaceutical analysis · 2025
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  11. Pharmaceuticals (Basel, Switzerland) · 2024
    Article
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  14. Review
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  16. Article
  17. Article
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  20. 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

13 authors at 3 institutions in 2 countries.

Jie ZhaoHenan Key Laboratory of Chinese Medicine for Respiratory Disease, Collaborative Innovation Center for Respiratory Disease Diagnosis and Treatment & Chinese Medicine Development of Henan Province, Academy of Chinses Medical Sciences, Henan University of Chinese Medicine, Zhengzhou, Henan, China; School of Pharmaceutical Science, Hebei Medical University, Shijiazhuang, Hebei, China; Laboratory of Metabolism, National Cancer Institute, Bethesda, MD, USA.
Cen XieLaboratory of Metabolism, National Cancer Institute, Bethesda, MD, USA; State Key Laboratory of Drug Research, Shanghai Institute of Materia Medica, Chinese Academy of Sciences, Shanghai, China.
Kanglong WangState Key Laboratory of Drug Research, Shanghai Institute of Materia Medica, Chinese Academy of Sciences, Shanghai, China.
Shogo TakahashiLaboratory of Metabolism, National Cancer Institute, Bethesda, MD, USA.
Kristopher W KrauszLaboratory of Metabolism, National Cancer Institute, Bethesda, MD, USA.
Dasheng LuLaboratory of Metabolism, National Cancer Institute, Bethesda, MD, USA.
Qiong WangLaboratory of Metabolism, National Cancer Institute, Bethesda, MD, USA.
Yuhong LuoLaboratory of Metabolism, National Cancer Institute, Bethesda, MD, USA.
Xianqiong GongLaboratory of Metabolism, National Cancer Institute, Bethesda, MD, USA.
Xiyan MuSchool of Pharmaceutical Science, Hebei Medical University, Shijiazhuang, Hebei, China.
Qiao WangSchool of Pharmaceutical Science, Hebei Medical University, Shijiazhuang, Hebei, China. Electronic address: qiaowang88@hotmail.com.
Suwen SuDepartment of Pharmacology, Hebei Medical University, Shijiazhuang, Hebei, China. Electronic address: suswmk@hebmu.edu.cn.
Frank J GonzalezLaboratory of Metabolism, National Cancer Institute, Bethesda, MD, USA.
National Cancer Institute · USHebei Medical University · CNChinese Academy of Sciences · CN

Funding

Xenobiotic ReceptorsZIABC005708 · NCI · DIVISION OF BASIC SCIENCES - NCI · PI GONZALEZ, FRANK J · 2009 to 2025
$16.4M
Intramural NIH HHS ZIA BC005708
6 · The paper itself

Abstract

Triptolide, a major active component of Triptergium wilfordii Hook. f, is used in the treatment of autoimmune disease. However, triptolide is associated with severe adverse reactions, especially hepatotoxicity, which limits its clinical application. To examine the underlying mechanism of triptolide-induced liver injury, a combination of dose- and time-dependent toxic effects, RNA-seq and metabolomics were employed. Triptolide-induced toxicity occurred in a dose- and time-dependent manners and was characterized by apoptosis and not necroptosis. Transcriptomics profiles of the dose-dependent response to triptolide suggested that PI3K/AKT, MAPK, TNFα and p53 signaling pathways were the vital steps in triptolide-induced hepatocyte apoptosis. Metabolomics further revealed that glycerophospholipid, fatty acid, leukotriene, purine and pyrimidine metabolism were the major metabolic alterations after triptolide exposure. Finally, acylcarnitines were identified as potential biomarkers for the early detection of triptolide-induced liver injury.

Indexed as

Chemical and Drug Induced Liver InjuryAnimalsApoptosisDiterpenesDose-Response Relationship, DrugEpoxy CompoundsGene Expression ProfilingMetabolomeMetabolomicsMiceMice, Inbred C57BLMice, KnockoutNecroptosisPhenanthrenesTranscriptomeDiterpenesEpoxy CompoundsPhenanthrenestriptolideAcylcarnitineApoptosisMetabolomicsTranscriptomicsTriptolide

Identifiers

PMID32835833
PMCPMC7783549
OpenAlexW3081173988

What OpenQuestion holds

Textmetadata
LicenceTDM
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.