Evidence map›Paper›PMID 42848251›Full record

ReviewMolecular biology reports2026

Deoxynivalenol-induced cellular signal transduction: research progress on toxicological effects, molecular mechanisms, and biological intervention strategies.

Doudou Feng, Suxian Liu, Jingjing Zhao, Yukai Lin, Siyang Li, Minghui Li, Ke Ding, Lei Wang, Ruibiao Wang

Abstract readReview
PubMed Publisher
In one paragraph

Review in Molecular biology 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.

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

9 authors.

Doudou FengCollege of Animal Science and Technology, Henan Institute of Science and Technology, Xinxiang, 453003, China.
Suxian LiuCollege of Animal Science and Technology, Henan Institute of Science and Technology, Xinxiang, 453003, China.
Jingjing ZhaoCollege of Animal Science and Technology, Henan Institute of Science and Technology, Xinxiang, 453003, China.
Yukai LinCollege of Animal Science and Technology, Henan Institute of Science and Technology, Xinxiang, 453003, China.
Siyang LiCollege of Animal Science and Technology, Henan Institute of Science and Technology, Xinxiang, 453003, China.
Minghui LiCollege of Animal Science and Technology, Henan Institute of Science and Technology, Xinxiang, 453003, China.
Ke DingCollege of Animal Science and Technology, Henan Institute of Science and Technology, Xinxiang, 453003, China.
Lei WangCollege of Animal Science and Technology, Henan Institute of Science and Technology, Xinxiang, 453003, China.
Ruibiao WangCollege of Animal Science and Technology, Henan Institute of Science and Technology, Xinxiang, 453003, China. wangrb2023@hist.edu.cn.

Funding

National Key R&D Program of China 2021YFD1301200Science and Technology Innovative Research Team in Higher Educational Institutions of Henan Province 24IRTSTHN035This work was supported by National Natural Science Foundation of China 32473037
6 · The paper itself

Abstract

Deoxynivalenol (DON) is an important mycotoxin that contaminates cereal grains and poses serious threats to livestock and poultry production and human health. This review systematically summarizes the cytotoxicity of DON in the intestinal, immune, nervous, and reproductive systems. Particular emphasis is placed on the mechanism in which the direct ribotoxic stress response (direct RSR) acts as the initial trigger, followed by an imbalance in signaling networks and secondary amplification of ROS and endoplasmic reticulum (ER) stress. Through crosstalk among the MAPK, PI3K/AKT/mTOR, NF-κB, JAK2/STAT3, Nrf2/Keap1, and Wnt/β-catenin pathways, these processes further amplify mitochondrial damage, inflammation, apoptosis, and ferroptosis. This review also summarizes how probiotics, postbiotics, and their metabolites alleviate DON toxicity by regulating apoptosis, protecting the intestinal barrier, mediating signaling pathways, and releasing bioactive metabolites. Current bottlenecks are highlighted, including the unclear structures and toxicology of degradation products, poor intestinal stability, strong strain specificity, and overestimation of in vitro efficacy. Future directions are then discussed to provide a basis for mechanistic studies on the combined effects of DON and intervention agents.

Indexed as

Signal TransductionTrichothecenesAnimalsApoptosisEndoplasmic Reticulum StressHumansMycotoxinsReactive Oxygen SpeciesdeoxynivalenolMycotoxinsReactive Oxygen SpeciesTrichothecenesCytotoxicityDeoxynivalenol (DON)Direct Ribotoxic Stress Response (direct RSR)Pathway synergyProbiotic interventionSignaling pathways

Identifiers

What OpenQuestion holds

Textmetadata
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.