ArticleOxidative medicine and cellular longevity2021
Emodin-Induced Oxidative Inhibition of Mitochondrial Function Assists BiP/IRE1
Article in Oxidative medicine and cellular longevity, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 23 citations in OpenAlex.
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- hsa_circ_0004771-Targeted Adsorption of miR-429 Mediates ATP2A2 Expression to Attenuate Endoplasmic Reticulum Stress and Mitochondrial Dysfunction During Myocardial Infarction.Applied biochemistry and biotechnology · 2025Article
- The role of the ER stress sensor IRE1 in cardiovascular diseases.Molecular and cellular biochemistry · 2025Review
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- Esophageal cancer stem cells reduce hypoxia-induced apoptosis by inhibiting the GRP78-perk-eIF2α-ATF4-CHOP pathwayJournal of gastrointestinal oncology · 2023Article
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- Tripartite motif 25 ameliorates doxorubicin-induced cardiotoxicity by degrading p85α.Cell death & disease · 2022Article
- Role of ER Stress in Xenobiotic-Induced Liver Diseases and Hepatotoxicity.Oxidative medicine and cellular longevity · 2022Review
- Reactive Oxygen Species in Cardiovascular Calcification: Role of Medicinal Plants.Frontiers in pharmacology · 2022Review
- IRE1 signaling regulates chondrocyte apoptosis and death fate in the osteoarthritis.Journal of cellular physiology · 2022Review
- Vitexin ameliorates glycochenodeoxycholate-induced hepatocyte injury through SIRT6 and JAK2/STAT3 pathways.Iranian journal of basic medical sciences · 2021Article
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Authors and funding
13 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cassiae Semen is a widely used herbal medicine and a popular edible variety in many dietary or health beverage. Emerging evidence disclosed that improper administration of Cassiae Semen could induce obvious liver injury, which is possibly attributed to emodin, one of the bioactive anthraquinone compounds in Cassiae Semen, which caused hepatotoxicity, but the underlying mechanisms are not completely understood. Hence, the present study firstly explored the possible role of oxidative stress-mediated mitochondrial dysfunction and ER stress in emodin-cause apoptosis of L02 cells, aiming to elaborate possible toxic mechanisms involved in emodin-induced hepatotoxicity. Our results showed that emodin-induced ROS activated ER stress and the UPR via the BiP/IRE1
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