ReviewOxidative medicine and cellular longevity2021
Ferroptosis Mediated by Lipid Reactive Oxygen Species: A Possible Causal Link of Neuroinflammation to Neurological Disorders.
Review 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 59 papers.
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Who cites it
59 citing papers in PubMed, 107 citations in OpenAlex.
- Comorbid mechanisms of neuroinflammation and astrocytic ferroptosis in neurological disorders: A vicious cycle (Review).Biomedical reports · 2026Review
- Interconnected cell death pathways: central mechanisms and therapeutic targets in impaired follicular development of polycystic ovary syndrome.Journal of ovarian research · 2026Review
- The aging gut-glia-immune axis in alzheimer's disease: microbiome-derived mediators of neuroinflammation and therapeutic innovation.GeroScience · 2026Review
- Research Progress on Ferroptosis Regulation of Female Reproduction.Biological trace element research · 2026Review
- Processing-induced changes in neuroprotective components and mechanisms of gardeniae fructus: integrating UPLC-Q-TOF-MS/MS, network pharmacology, and in vitro analysis.Bioresources and bioprocessing · 2026Article
- Ferroptosis associated with secondary brain damage induced by hypertensive underlying biological processes in intracerebral hemorrhage and therapeutic prospects.European journal of medical research · 2026Review
- Ferroptosis-neuroinflammation interplay: mechanistic pathways and therapeutic opportunities in central nervous system disorders.Frontiers in aging neuroscience · 2026Review
- Ferroptosis-immune crosstalk in CNS diseases: mechanisms and translational insights.Frontiers in immunology · 2026Review
- Histone lactylation-mediated glycolysis-ferroptosis axis in neurological diseases.Frontiers in molecular neuroscience · 2026Review
- Diabetes, Alzheimer's Disease Risk Factors, and the Cafeteria Diet: A Comprehensive Review.Current neuropharmacology · 2026Review
- Targeting ferroptosis in ocular diseases: mechanisms, clinical implications, and therapeutic horizons.International journal of ophthalmology · 2026Review
- Article
- Management and Prevention of Neurodegenerative Disorders: Can Antioxidant-Rich Dietary Interventions Help?Antioxidants (Basel, Switzerland) · 2025Review
- Ferroptosis and Metabolic Dysregulation: Emerging Chemical Targets in Cancer and Infection.Molecules (Basel, Switzerland) · 2025Review
- Synthesis of thiosemicarbazone derivatives and evaluation of their cytotoxicity with emphasis on ferroptosis biomarkers; anResearch in pharmaceutical sciences · 2025Article
- Multifunctional astragalus polysaccharide composited microneedle promotes oral ulcers healing by inhibiting ferroptosis via Nrf2/HO-1/SLC7A11 axis.Materials today. Bio · 2025Article
- Peripheral blood heat shock protein 27 correlates with information processing speed and executive function, potentially serving as a marker for mild cognitive impairment in patients with type 2 diabetes mellitus.Diabetology & metabolic syndrome · 2025Article
- Electroacupuncture Inhibits Ferroptosis by Modulating Iron Metabolism and Oxidative Stress to Alleviate Cerebral Ischemia-Reperfusion Injury.Journal of molecular neuroscience : MN · 2025Article
- Ferroptosis and Iron Homeostasis: Molecular Mechanisms and Neurodegenerative Disease Implications.Antioxidants (Basel, Switzerland) · 2025Review
- Cytolethal distending toxin from Glaesserella parasuis induces ferroptosis in porcine alveolar macrophages and mice.Veterinary research · 2025Article
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Increasing evidence indicates a possible causal link between neuroinflammation and neurological disorders, including Alzheimer's disease (AD), Parkinson's disease (PD), Huntington's disease (HD), and stroke. A putative mechanism underlying such a link can be explained by ferroptosis. Current studies have shown that disturbances of iron homeostasis, glutamate excitatory toxicity, lipid reactive oxygen species (ROS), and other manifestations related to ferroptosis can be detected in several neurological disorders caused by neuroinflammation. To date, compelling evidence indicates that damage-associated molecular pattern (DAMP) molecules (e.g., ROS) produced in the process of ferroptosis activate glial cells by activating neuroimmune pathways and then produce a series of inflammatory factors which contribute to neurological disorders. Our review article provides a current view of the involvement of ferroptosis or ROS in the pathological process of neuroinflammation, the effects of neuroinflammation mediated by ferroptosis in neurological disorders, a better understanding of the mechanisms underlying ferroptosis participates in neuroinflammation, and the potential treatments for neurological disorders. In addition, further research on the mechanisms of ferroptosis as well as the link between ferroptosis and neuroinflammation will help provide new targets for treatment.
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Registered trials
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.