Trial reportRedox biology2018
Iron-loaded transferrin (Tf) is detrimental whereas iron-free Tf confers protection against brain ischemia by modifying blood Tf saturation and subsequent neuronal damage.
Trial report in Redox biology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 papers.
What it found
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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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
49 citing papers in PubMed, 75 citations in OpenAlex.
- Iron, Copper, and Zinc Dyshomeostasis in Cardiovascular and Cerebrovascular Diseases: Redox Mechanisms, Evidence Levels, and Translational Prospects.International journal of molecular sciences · 2026Review
- Prediction of early neurological deterioration using quantitative susceptibility mapping in small artery occlusion ischemic stroke.IBRO neuroscience reports · 2026Article
- The association of a common HFE gene variant with stroke disability utilizing predictive machine learning and electronic health records.Scientific reports · 2026Article
- PEBP1 inhibition as a therapeutic target for neurological recovery in ischemic stroke.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2026Article
- Non-specific Protein and Peptide Antibacterial Factors of Mammals.The protein journal · 2026Review
- Integrated 3D-Printed Microfluidic Device for Immunocapture and Electrochemical Assessment of Transferrin Saturation inACS sensors · 2026Article
- Review
- Ferroptosis in cancer: metabolism, mechanisms and therapeutic prospects.Molecular cancer · 2025Review
- Harnessing Mitochondrial Function for Post-Stroke Rehabilitation: Unlocking Antioxidant Power.Antioxidants (Basel, Switzerland) · 2025Review
- Acupuncture Alleviates Blood-Brain Barrier Damage After Delayed rtPA Thrombolysis for Acute Ischemic Stroke by Regulating Ferroptosis.Brain and behavior · 2025Article
- Empagliflozin Inhibits Neuronal Ferroptosis Induced by Oxygen-Glucose Deprivation/Reoxygenation by Activating the Nrf2/HO-1 Pathway.Molecular neurobiology · 2025Article
- Molecular mechanisms of programmed cell death and potential targeted pharmacotherapy in ischemic stroke (Review).International journal of molecular medicine · 2025Review
- Exploring the causal relationship between iron status and subarachnoid hemorrhage based on two sample mendelian randomization.Scientific reports · 2025Article
- Exploring the Role of Ferroptosis-Related Circular RNAs in Subarachnoid Hemorrhage.Molecular biotechnology · 2025Review
- Decoding ferroptosis in ischemic stroke: key genes and the therapeutic potential of acupuncture.Frontiers in aging neuroscience · 2025Article
- Modulating Ferroptosis: A Novel Approach to Promote Neural Repair in Brain Injury.Current neuropharmacology · 2025Review
- Targeting ferroptosis with natural products in stroke: therapeutic mechanisms and translational opportunities.Frontiers in pharmacology · 2025Review
- Iron homeostasis and ferroptosis in human diseases: mechanisms and therapeutic prospects.Signal transduction and targeted therapy · 2024Review
- Pathophysiological changes of muscle after ischemic stroke: a secondary consequence of stroke injury.Neural regeneration research · 2024Review
- Ferroptosis and endoplasmic reticulum stress in ischemic stroke.Neural regeneration research · 2024Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
14 authors at 7 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Despite transferrin being the main circulating carrier of iron in body fluids, and iron overload conditions being known to worsen stroke outcome through reactive oxygen species (ROS)-induced damage, the contribution of blood transferrin saturation (TSAT) to stroke brain damage is unknown. The objective of this study was to obtain evidence on whether TSAT determines the impact of experimental ischemic stroke on brain damage and whether iron-free transferrin (apotransferrin, ATf)-induced reduction of TSAT is neuroprotective. We found that experimental ischemic stroke promoted an early extravasation of circulating iron-loaded transferrin (holotransferrin, HTf) to the ischemic brain parenchyma. In vitro, HTf was found to boost ROS production and to be harmful to primary neuronal cultures exposed to oxygen and glucose deprivation. In stroked rats, whereas increasing TSAT with exogenous HTf was detrimental, administration of exogenous ATf and the subsequent reduction of TSAT was neuroprotective. Mechanistically, ATf did not prevent extravasation of HTf to the brain parenchyma in rats exposed to ischemic stroke. However, ATf in vitro reduced NMDA-induced neuronal uptake of HTf and also both the NMDA-mediated lipid peroxidation derived 4-HNE and the resulting neuronal death without altering Ca
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.