ArticleArchives of toxicology2022
Deoxynivalenol induces caspase-3/GSDME-dependent pyroptosis and inflammation in mouse liver and HepaRG cells.
Article in Archives of toxicology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 51 citations in OpenAlex.
- Recent advances in the mechanism of deoxynivalenol-induced hepatotoxicity and protective strategies.Archives of toxicology · 2026Review
- Targeting pyroptosis in metabolic dysfunction-associated steatotic liver disease: from molecular mechanisms to therapeutic innovation.Molecular biology reports · 2026Review
- Article
- Bacillus velezensis mitigates deoxynivalenol-induced intestinal inflammation and liver injury via modulating the gut microbiota.NPJ science of food · 2026Article
- Pharmacological Targeting of NRF2 Represents a Promising Therapeutic Approach for Pyroptosis-Related Non-Alcoholic Fatty Liver Disease.Current medicinal chemistry · 2026Review
- Lipin3 deficiency promotes hepatocyte ferroptosis and pyroptosis via activating JAK1-STAT3 pathway during acetaminophen induced acute liver injury.Molecular biomedicine · 2025Article
- Article
- The PGC-1α/SIRT3 pathway mediates the effect of DON on mitochondrial autophagy and liver injury in mice.Mycotoxin research · 2025Article
- [Research progress in the role of caspaseZhong nan da xue xue bao. Yi xue ban = Journal of Central South University. Medical sciences · 2025Review
- Protective effects of bone marrow mesenchymal stem cell-derived exosomes loaded cerium dioxide nanoparticle against deoxynivalenol-induced liver damage.Journal of nanobiotechnology · 2025Article
- GSDME in cardiovascular diseases: research system and contemporary progress.Frontiers in immunology · 2025Review
- Chlorogenic acid alleviates IPEC-J2 pyroptosis induced by deoxynivalenol by inhibiting activation of the NF-κB/NLRP3/caspase-1 pathway.Journal of animal science and biotechnology · 2024Article
- Mechanisms and cross-talk of regulated cell death and their epigenetic modifications in tumor progression.Molecular cancer · 2024Review
- Article
- The Novel Role of the NLRP3 Inflammasome in Mycotoxin-Induced Toxicological Mechanisms.Veterinary sciences · 2024Review
- The inflammatory injury of porcine small intestinal epithelial cells induced by deoxynivalenol is related to the decrease in glucose transport.Journal of animal science · 2024Article
- Advances in research on the impact and mechanisms of pathogenic microorganism infections on pyroptosis.Frontiers in microbiology · 2024Review
- Proinflammatory cytokines interleukin-18 and interleukin-6 mediate anorexia induction by trichothecene deoxynivalenol and its congeners.Frontiers in veterinary science · 2024Article
- Real-life exposure to Fusarium toxins deoxynivalenol and zearalenone triggers apoptosis and activates NLRP3 inflammasome in bovine primary theca cells.Mycotoxin research · 2023Article
- Article
Corrections and comments
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
Abstract
Deoxynivalenol (DON), a frequent food and feed contaminant, poses a severe threat to human and livestock health. Some studies have demonstrated that DON could induce liver damage and cell death. However, novel cell death styles and detailed mechanisms to explain DON-induced liver inflammatory injury are still lacking. Here, we found both chronic and subacute oral administration of DON (3 mg/kg for 4 weeks and 4 mg/kg for 8 days) induced mouse liver inflammatory injury and activated caspase-3, PARP and gasdermin E (GSDME), which were inhibited by caspase-3 inhibitor Z-DEVD and Ac-DEVD. In vitro, HepaRG cells showed typical pyroptotic characteristics after 32 and 64 μM DON exposure for 24 h, including balloon-like bubbling emerging, release of lactate dehydrogenase (LDH), secretion of IL-1β and IL-6 and activation of caspase-3 and GSDME. Furthermore, knocking down GSDME and inhibiting caspases activity by Z-VAD and Z-DEVD dramatically blocked DON-induced pyroptotic characteristics, while over-expressed GSDME prompted that. These data demonstrate that caspase-3/GSDME pathway plays a key factor in DON-induced pyroptosis and inflammation in liver. Interestingly, knocking down GSDME could inhibit DON-induced pyroptosis but prompt DON-induced apoptosis, while opposite results were obtained when over-expressed GSDME, indicating the critical role of GSDME in DON-induced crosstalk between apoptosis and pyroptosis. Taken together, our data determine DON-induced caspase-3/GSDME-dependent pyroptosis in liver and its role in DON-induced liver inflammatory injury, which provide a novel mechanistic view into DON-induced hepatotoxicity and may offer a new target to reduce latent harm of DON to both humans and animals.
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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 OpenQuestion graph.