ArticleBiological trace element research2024
p53-Mediated Mitochondrial Translocation of EI24 Triggered by ER Stress Plays an Important Role in Arsenic-Induced Liver Damage via Activating Mitochondrial Apoptotic Pathway.
Article in Biological trace element research, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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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.
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Who cites it
3 citing papers in PubMed, 3 citations in OpenAlex.
- Dietary genistein alleviates arsenic trioxide-induced ionoregulatory disruption, oxidative and endoplasmic reticulum stress, and apoptotic gene expression in the gills and kidneys of Oreochromis niloticus.Veterinary research communications · 2026Article
- Biological significance, molecular mechanisms and clinical potential of EI24 in cancer.Chinese medical journal · 2026Review
- Yunweiling alleviates functional constipation: integrating network pharmacology and experimental study.Animal models and experimental medicine · 2025Article
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Chronic arsenic poisoning is a public health problem worldwide. In addition to skin lesions, the detrimental effect of arsenic poisoning on liver damage is one of the major issues. Our previous studies demonstrated that endoplasmic reticulum (ER) stress and p53 were associated with arsenic-induced liver damage. Literature has shown that EI24 is involved in hepatocyte hypertrophy; however, the underlying role and mechanism in arsenic-induced liver damage have not been fully elucidated. In this study, we explored the role of ER stress, p53, and EI24 as well as the regulatory relationship in arsenic poisoning populations and L-02 cells treated with distinct concentration NaAsO
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