ArticleBrain and behavior2022
The protective mechanism of protein kinase R to inhibit neuronal ferroptosis in cerebral injury from subarachnoid hemorrhage.
Article in Brain and behavior, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed, 6 citations in OpenAlex.
- Unravelling the role of protein kinase R (PKR) in neurodegenerative disease: a review.Molecular biology reports · 2025Review
- The PERK-eIF2α-ATF4 Axis Is Involved in Mediating ER-Stress-Induced Ferroptosis via DDIT4-mTORC1 Inhibition and Acetaminophen-Induced Hepatotoxicity.Antioxidants (Basel, Switzerland) · 2025Article
- Pharmacological Inhibition of Ferroptosis as a Therapeutic Target for Neurodegenerative Diseases and Strokes.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2023Review
- The protective mechanism of protein kinase R to inhibit neuronal ferroptosis in cerebral injury from subarachnoid hemorrhage.Brain and behavior · 2022Article
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
purposeTo investigate the role and mechanism of protein kinase R (PKR) in subarachnoid hemorrhage (SAH)-mediated ferroptosis.
methodsA rat SAH model was constructed and treated with PKR inhibitor C16 to observe SAH and neurological impairment in rats and to detect malonaldehyde (MDA), iron ions content, ferritin heavy polypeptide 1 (FTH1) and glutathione peroxidase 4 (GPX4), and other related ferroptosis indicators in brain tissue. RNA sequencing analysis was used to investigate the mechanism of PKR, affecting the ferroptosis network of SAH.
resultsSAH caused severe fundic hemorrhage, neurological impairment, MDA and iron ion accumulation, and significant decrease in GPX4 and FTH1 levels in rats. C16 treatment significantly improved the above signs caused by SAH. By RNA-seq analysis, brain tissue of SAH-treated rats with SAH and C16 differentially expressed mRNA target genes enriched in stress response and organic developmental signaling pathways.
conclusionInhibition of PKR may improve cerebral injury after SAH by inhibiting ferroptosis, and RNA sequencing staged its mechanism of action may be related to the stress response.
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