ArticleCommunications biology2025
Deoxynivalenol induces ferroptosis via inhibiting glycolysis-H3K18la-STEAP3 axis to promote ovary damage in piglets.
Article in Communications biology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
What it found
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Who cites it
7 citing papers in PubMed.
- Deoxynivalenol-induced cellular signal transduction: research progress on toxicological effects, molecular mechanisms, and biological intervention strategies.Molecular biology reports · 2026Review
- Lactate-dependent regulation of ferroptosis: redox homeostasis, lactylation, and translational perspectives.Apoptosis : an international journal on programmed cell death · 2026Review
- Restoring glucose metabolic homeostasis to attenuate ovarian aging: mechanisms and clinical prospects.Journal of ovarian research · 2026Review
- Lactate in ruminant health: metabolic roles and the emerging significance of lactylation.Journal of animal science and biotechnology · 2026Review
- Effects of Chlorogenic Acid on Deoxynivalenol (DON)-Induced Ferroptosis in Porcine Alveolar Macrophages.Toxins · 2026Article
- Transcriptomic Analysis of Fermented Chinese Chive Selectively Attenuating Deoxynivalenol-Induced Ovarian Toxicity in Mice.Antioxidants (Basel, Switzerland) · 2026Article
- Proteomic analysis reveals the molecular mechanisms of deoxynivalenol-induced injury in the jejunum of piglets.BMC genomics · 2026Article
Corrections and comments
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Authors and funding
12 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Deoxynivalenol (DON), a prevalent mycotoxin in contaminated feed, compromises ovarian function through dual disruption of redox homeostasis and metabolic networks. However, the precise mechanisms underlying DON-induced toxicity and effective strategies to mitigate its reproductive consequences remain incompletely understood. This study reveals the molecular mechanism by which DON induces ferroptosis in porcine granulosa cells through the glycolysis-H3K18la-STEAP3 axis and elucidates how melatonin alleviates DON toxicity via metabolic reprogramming. Multi-omics analyses demonstrate that DON exposure disrupts glycolysis, reduces lactate, and diminished H3K18la. This process is also mediated by the downregulation of P300, a key writer of lactylation, which collectively suppress H3K18la. The loss of H3K18la decreased STEAP3 expression, intracellular iron accumulation, elevated lipid peroxidation, and downregulation of GPX4, ultimately triggering ferroptosis. Furthermore, melatonin restores H3K18la and STEAP3 expression both in vitro and vivo, thereby suppressing ferroptosis and reducing oxidative stress. These findings provide novel molecular targets and therapeutic strategies for DON intoxication.
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Registered trials
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.