ArticleFree radical biology & medicine2009
Neurotoxic lipid peroxidation species formed by ischemic stroke increase injury.
Article in Free radical biology & medicine, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
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Who cites it
25 citing papers in PubMed, 44 citations in OpenAlex.
- Dynamic metabolic programming of monocyte-derived cells defines immunity in CNS disease.Brain : a journal of neurology · 2026Review
- Therapeutic spectrum of Piperine in ischemic stroke: a literature review.Molecular biology reports · 2025Review
- Exploring Lysophosphatidylcholine as a Biomarker in Ischemic Stroke: The Plasma-Brain Disjunction.International journal of molecular sciences · 2024Article
- Ischemic Brain Injury: Involvement of Lipids in the Pathophysiology of Stroke and Therapeutic Strategies.Antioxidants (Basel, Switzerland) · 2024Review
- Reinventing the Penumbra - the Emerging Clockwork of a Multi-modal Mechanistic Paradigm.Translational stroke research · 2023Review
- Targeting foam cell formation to improve recovery from ischemic stroke.Neurobiology of disease · 2023Review
- L-F001, a Multifunctional Fasudil-Lipoic Acid Dimer Prevents RSL3-Induced FerroptosisFrontiers in cellular neuroscience · 2022Article
- Enhanced thioredoxin, glutathione and Nrf2 antioxidant systems by safflower extract and aceglutamide attenuate cerebral ischaemia/reperfusion injury.Journal of cellular and molecular medicine · 2020Article
- Fourier-Transform Infrared Imaging Spectroscopy and Laser Ablation -ICPMS New Vistas for Biochemical Analyses of Ischemic Stroke in Rat Brain.Frontiers in neuroscience · 2018Article
- Neuroprotection of ischemic preconditioning is mediated by thioredoxin 2 in the hippocampal CA1 region following a subsequent transient cerebral ischemia.Brain pathology (Zurich, Switzerland) · 2017Article
- NaHS Protects against the Impairments Induced by Oxygen-Glucose Deprivation in Different Ages of Primary Hippocampal Neurons.Frontiers in cellular neuroscience · 2017Article
- Clinical perspective on oxidative stress in sporadic amyotrophic lateral sclerosis.Free radical biology & medicine · 2013Review
- Polyunsaturated fatty acid metabolism signature in ischemia differs from reperfusion in mouse intestine.PloS one · 2013Article
- Article
- Transgenic overexpression of peroxiredoxin-2 attenuates ischemic neuronal injury via suppression of a redox-sensitive pro-death signaling pathway.Antioxidants & redox signaling · 2012Article
- Metabolic multianalyte microphysiometry reveals extracellular acidosis is an essential mediator of neuronal preconditioning.ACS chemical neuroscience · 2012Article
- Article
- Isoprostane generation and function.Chemical reviews · 2011Review
- Significance of brain tissue oxygenation and the arachidonic acid cascade in stroke.Antioxidants & redox signaling · 2011Review
- Neuron specific metabolic adaptations following multi-day exposures to oxygen glucose deprivation.Biochimica et biophysica acta · 2010Article
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 2 countries.
Funding
Abstract
Stroke is the third leading cause of death in the United States, yet no neuroprotective agents for treatment are clinically available. There is a pressing need to understand the signaling molecules that mediate ischemic cell death and identify novel neuroprotective targets. Cyclopentenone isoprostanes (IsoPs), formed after free radical-mediated peroxidation of arachidonic acid, are used as markers of stress, but their bioactivity is poorly understood. We have recently shown that 15-A(2t)-IsoP is a potent neurotoxin in vitro and increases the free radical burden in neurons. In this work, we demonstrate that 15-A(2t)-IsoP is abundantly produced in stroke-infarcted human cortical tissue. Using primary neuronal cultures we found that minimally toxic exposure to 15-A(2t)-IsoP does not alter ATP content, but in combination with oxygen glucose deprivation resulted in a significant hyperpolarization of the mitochondrial membrane and dramatically increased neuronal cell death. In the presence of Ca(2+), 15-A(2t)-IsoP led to a rapid induction of the permeability transition pore and release of cytochrome c. Taken with our previous work, these data support a model in which ischemia causes generation of reactive oxygen species, calcium influx, lipid peroxidation, and 15-A(2t)-IsoP formation. These factors combine to enhance opening of the permeability transition pore leading to cell death subsequent to mitochondrial cytochrome c release. These data are the first documentation of significant 15-A(2t)-IsoP formation after acute ischemic stroke and suggest that the addition of 15-A(2t)-IsoP to in vitro models of ischemia may help to more fully recapitulate stroke injury.
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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.