ArticleMolecules (Basel, Switzerland)2016
Phosphorylation of Akt by SC79 Prevents Iron Accumulation and Ameliorates Early Brain Injury in a Model of Experimental Subarachnoid Hemorrhage.
Article in Molecules (Basel, Switzerland), 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 23 citations in OpenAlex.
- Pharmacological intervention of Chinese medicine via regulating ferroptosis in gastric cancer.Chinese medicine · 2026Review
- Structural insights of AKT and its activation mechanism for drug development.Molecular diversity · 2025Review
- Targeting ferroptosis in cancer stem cells: A novel strategy to improve cancer treatment.Genes & diseases · 2025Review
- Akt activator SC79 prevents impaired subsequent LTP in the hippocampus of hypothyroid rats.Experimental brain research · 2025Article
- Correction: Hao et al. Phosphorylation of Akt by SC79 Prevents Iron Accumulation and Ameliorates Early Brain Injury in a Model of Experimental Subarachnoid Hemorrhage.Molecules (Basel, Switzerland) · 2025Article
- Research progress of early brain Injury in subarachnoid hemorrhage from 2004 to 2024: a bibliometric analysis.Neurosurgical review · 2025Review
- Iron Metabolism and Ferroptosis in Early Brain Injury after Subarachnoid Haemorrhage.Molecular neurobiology · 2024Review
- Article
- Mechanisms of Ferritinophagy and Ferroptosis in Diseases.Molecular neurobiology · 2024Review
- The role of mitochondria in the recovery of neurons after injury.Neural regeneration research · 2023Article
- An Update on Antioxidative Stress Therapy Research for Early Brain Injury After Subarachnoid Hemorrhage.Frontiers in aging neuroscience · 2021Review
- Article
- Iron regulatory protein deficiency compromises mitochondrial function in murine embryonic fibroblasts.Scientific reports · 2018Article
- SC79 protects dopaminergic neurons from oxidative stress.Oncotarget · 2018Article
- MIND4-17 protects retinal pigment epithelium cells and retinal ganglion cells from UV.Oncotarget · 2017Article
- Article
Corrections and comments
- Erratum issued
Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Previous studies have demonstrated that activation of Akt may alleviate early brain injury (EBI) following subarachnoid hemorrhage (SAH). This study is undertaken to determine whether iron metabolism is involved in the beneficial effect of Akt activation after SAH. Therefore, we used a novel molecule, SC79, to activate Akt in an experimental Sprague-Dawley rat model of SAH. Rats were randomly divided into four groups as follows: sham, SAH, SAH + vehicle, SAH + SC79. The results confirmed that SC79 effectively enhanced the defense against oxidative stress and alleviated EBI in the temporal lobe after SAH. Interestingly, we found that phosphorylation of Akt by SC79 reduced cell surface transferrin receptor-mediated iron uptake and promoted ferroportin-mediated iron transport after SAH. As a result, SC79 administration diminished the iron content in the brain tissue. Moreover, the impaired Fe-S cluster biogenesis was recovered and loss of the activities of the Fe-S cluster-containing enzymes were regained, indicating that injured mitochondrial functions are restored to healthy levels. These findings suggest that disrupted iron homeostasis could contribute to EBI and Akt activation may regulate iron metabolism to relieve iron toxicity, further protecting neurons from EBI after SAH.
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