Evidence map›Paper›PMID 33505311›Full record

ReviewFrontiers in pharmacology2020

Contamination of Aflatoxins Induces Severe Hepatotoxicity Through Multiple Mechanisms.

Zhenglai Hua, Rui Liu, Youwen Chen, Guangzhi Liu, Chenxi Li, Yurong Song, Zhiwen Cao, Wen Li, Weifeng Li, Cheng Lu and 1 more

Open access · goldAbstract readReview
In one paragraph

Review in Frontiers in pharmacology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed
3.2field-weighted citation impact, top 7% 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

31 citing papers in PubMed, 68 citations in OpenAlex.

  1. Aflatoxin exposure and health impacts: global burden and advances in detection technologies.Genes and environment : the official journal of the Japanese Environmental Mutagen Society · 2026
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  16. Journal of toxicology · 2025
    Article
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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

11 authors at 2 institutions in 1 country.

Zhenglai HuaSchool of Chinese Materia Medica, Beijing University of Chinese Medicine, Beijing, China.
Rui LiuSchool of Chinese Materia Medica, Beijing University of Chinese Medicine, Beijing, China.
Youwen ChenSchool of Chinese Materia Medica, Beijing University of Chinese Medicine, Beijing, China.
Guangzhi LiuSchool of Chinese Materia Medica, Beijing University of Chinese Medicine, Beijing, China.
Chenxi LiSchool of Chinese Materia Medica, Beijing University of Chinese Medicine, Beijing, China.
Yurong SongSchool of Chinese Materia Medica, Beijing University of Chinese Medicine, Beijing, China.
Zhiwen CaoSchool of Chinese Materia Medica, Beijing University of Chinese Medicine, Beijing, China.
Wen LiSchool of Chinese Materia Medica, Beijing University of Chinese Medicine, Beijing, China.
Weifeng LiSchool of Chinese Materia Medica, Beijing University of Chinese Medicine, Beijing, China.
Cheng LuInstitute of Basic Research in Clinical Medicine, China Academy of Chinese Medical Sciences, Beijing, China.
Yuanyan LiuSchool of Chinese Materia Medica, Beijing University of Chinese Medicine, Beijing, China.
Beijing University of Chinese Medicine · CNChinese Academy of Medical Sciences & Peking Union Medical College · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Aflatoxins (AFs) are commonly contaminating mycotoxins in foods and medicinal materials. Since they were first discovered to cause "turkey X" disease in the United Kingdom in the early 1960s, the extreme toxicity of AFs in the human liver received serious attention. The liver is the major target organ where AFs are metabolized and converted into extremely toxic forms to engender hepatotoxicity. AFs influence mitochondrial respiratory function and destroy normal mitochondrial structure. AFs initiate damage to mitochondria and subsequent oxidative stress. AFs block cellular survival pathways, such as autophagy that eliminates impaired cellular structures and the antioxidant system that copes with oxidative stress, which may underlie their high toxicities. AFs induce cell death via intrinsic and extrinsic apoptosis pathways and influence the cell cycle and growth via microribonucleic acids (miRNAs). Furthermore, AFs induce the hepatic local inflammatory microenvironment to exacerbate hepatotoxicity via upregulation of NF-κB signaling pathway and inflammasome assembly in the presence of Kupffer cells (liver innate immunocytes). This review addresses the mechanisms of AFs-induced hepatotoxicity from various aspects and provides background knowledge to better understand AFs-related hepatoxic diseases.

Indexed as

aflatoxinscell deathcell survival pathwayhepatotoxicityinflammationmiRNAmitochondria

Identifiers

PMID33505311
PMCPMC7830880
OpenAlexW3119806864

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.