ArticleJournal of agricultural and food chemistry2024
Vitamin E Mitigates Apoptosis in Ovarian Granulosa Cells by Inhibiting Zearalenone-Induced Activation of the PERK/eIF-2α/ATF4/Chop Signaling Pathway.
Article in Journal of agricultural and food chemistry, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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.
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.
Who cites it
4 citing papers in PubMed.
- Vitamin E alleviates energy stress-induced injury in yak granulosa cells by blocking the AMPK/mTOR-mitophagy-ferroptosis axis.Journal of ovarian research · 2026Article
- Mazdutide Ameliorates Metabolic Dysfunction-Associated Steatotic Liver Disease by Modulating Endoplasmic Reticulum Stress, Improving Lipid Metabolism and Alleviating Inflammation.Pharmaceuticals (Basel, Switzerland) · 2026Article
- From gut-reproductive microbiota to ferroptosis: a comprehensive insight into the molecular-pathogenicity of endometriosis.Frontiers in immunology · 2026Review
- The cutting-edge progress of novel biomedicines in ovulatory dysfunction therapy.Acta pharmaceutica Sinica. B · 2025Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
A study aimed to investigate the signaling pathway of zearalenone (ZEA) leading to the apoptosis of ovarian granulosa cells (GCs) and explore the potential of vitamin E (VE) in alleviating ZEA-induced apoptosis of GCs. We constructed an apoptosis model for GCs based on exposure to the environmental toxin ZEA. Transcriptome analysis revealed that ZEA induced endoplasmic reticulum stress by activating the ATF4-Chop pathway. The addition of inhibitors targeting the estrogen receptor (ER) demonstrated that ZEA activates the ATF4-Chop pathway through ER-beta. As a strong antioxidant, VE is thought to mitigate ZEA-induced toxicity. Interestingly, molecular docking analysis at the PERK active site of the endoplasmic reticulum stress revealed a high binding capacity of VE. VE supplementation reduced apoptosis in GCs and decreased the expression of p-eIF-2α, ATF4, and Chop. Mouse tests also demonstrated that VE supplementation effectively mitigated ovarian dysfunction induced by ZEA, as evidenced by increased body weight gain, reduced oxidative stress, and decreased cell death. In summary, the present study demonstrates that ZEA activates the PERK-eIF-2α-ATF4-Chop pathway through ERβ, leading to endoplasmic reticulum stress and apoptosis of GCs. Conversely, VE inhibits the PERK/eIF-2α/ATF4/Chop signaling pathways, mitigating endoplasmic reticulum stress and improving ZEA-induced reproductive toxicity.
Indexed as
Identifiers
What OpenQuestion holds
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.