ArticleBiological trace element research2024
Role of PERK-Mediated Endoplasmic Reticulum Stress in Ferroptosis Caused by Hexavalent Chromium in Chicken Hepatocytes.
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 2 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
2 citing papers in PubMed, 4 citations in OpenAlex.
- Regulatory mechanisms of nutritional factors on melanin deposition in Taihe Silky Fowls: review.Animal bioscience · 2026Article
- Phloretin inhibits ferroptosis by restoring the antioxidant capacity of bovine adipose and muscle cells via the AMPK-PPAR signaling pathway.Stress biology · 2025Article
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
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Abstract
This study aimed to investigate whether Cr(VI) can induce ferroptosis in chicken hepatocytes and determine the role of PERK-mediated endoplasmic reticulum stress (ERS). First, a model of Cr(VI) poisoning was established by exposing chicken hepatocytes to Cr(VI). The levels of ferroptosis-related proteins, meanwhile, GSH, SOD, MDA, and lipid ROS, were measured. Furthermore, the expression of GRP78 and PERK proteins was examined. Changes in ERS and ferroptosis were evaluated by silencing the PERK gene. Results showed that Cr(VI) led to the accumulation of lipid ROS, decreased expression of GPX4 and HSP27, increased expression of COX2, and induced ferroptosis in chicken hepatocytes. Exposure to Cr(VI) increased the protein expression of GRP78 and PERK, and silencing of PERK worsened Cr(VI)-induced ferroptosis. In conclusion, Cr(VI) can induce ferroptosis in chicken hepatocytes, and PERK plays an important role as a negative regulator.
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