ReviewBrain pathology (Zurich, Switzerland)2005
Cyclopentenone eicosanoids as mediators of neurodegeneration: a pathogenic mechanism of oxidative stress-mediated and cyclooxygenase-mediated neurotoxicity.
Review in Brain pathology (Zurich, Switzerland), 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 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
16 citing papers in PubMed, 56 citations in OpenAlex.
- PGA1-induced apoptosis involves specific activation of H-Ras and N-Ras in cellular endomembranes.Cell death & disease · 2016Article
- Liquid Chromatography-Mass Spectrometry-Based In Vitro Metabolic Profiling Reveals Altered Enzyme Expressions in Eicosanoid Metabolism.Annals of laboratory medicine · 2016Article
- Prostaglandin J2: a potential target for halting inflammation-induced neurodegeneration.Annals of the New York Academy of Sciences · 2016Review
- Protein disulfide isomerase as a novel target for cyclopentenone prostaglandins: implications for hypoxic ischemic injury.The FEBS journal · 2015Article
- The isoprostanes--25 years later.Biochimica et biophysica acta · 2015Review
- Neuroinflammation and J2 prostaglandins: linking impairment of the ubiquitin-proteasome pathway and mitochondria to neurodegeneration.Frontiers in molecular neuroscience · 2014Review
- Clinical perspective on oxidative stress in sporadic amyotrophic lateral sclerosis.Free radical biology & medicine · 2013Review
- Lipid peroxidation biomarkers for evaluating oxidative stress and assessing antioxidant capacity in vivo.Journal of clinical biochemistry and nutrition · 2013Article
- Isoprostane generation and function.Chemical reviews · 2011Review
- ABC transporters in cancer: more than just drug efflux pumps.Nature reviews. Cancer · 2010Article
- Neurotoxic lipid peroxidation species formed by ischemic stroke increase injury.Free radical biology & medicine · 2009Article
- Subchronic infusion of the product of inflammation prostaglandin J2 models sporadic Parkinson's disease in mice.Journal of neuroinflammation · 2009Article
- Proteasome-caspase-cathepsin sequence leading to tau pathology induced by prostaglandin J2 in neuronal cells.Journal of neurochemistry · 2009Article
- Nitro-fatty acid metabolome: saturation, desaturation, beta-oxidation, and protein adduction.The Journal of biological chemistry · 2009Article
- Increase in PGE2 biosynthesis induces a Bax dependent apoptosis correlated to patients' survival in glioblastoma multiforme.Oncogene · 2007Article
- Review
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
The activation of cyclooxygenase enzymes in the brain has been implicated in the pathogenesis of numerous neurodegenerative conditions. Similarly, oxidative stress is believed to be a major contributor to many forms of neurodegeneration. These 2 distinct processes are united by a common characteristic: the generation of electrophilic cyclopentenone eicosanoids. These cyclopentenone compounds are defined structurally by the presence of an unsaturated carbonyl moiety in their prostane ring, and readily form Michael adducts with cellular thiols, including those found in glutathione and proteins. The cyclopentenone prostaglandins (PGs) PGA2, PGJ2, and 15-deoxy-delta(12,14) PGJ2, enzymatic products of cyclooxygenase-mediated arachidonic acid metabolism, exert a complex array of potent neurodegenerative, neuroprotective, and anti-inflammatory effects. Cyclopentenone isoprostanes (A2/J2-IsoPs), products of non-enzymatic, free radical-mediated arachidonate oxidation, are also highly bioactive, and can exert direct neurodegenerative effects. In addition, cyclopentenone products of docosahexaenoic acid oxidation (cyclopentenone neuroprostanes) are also formed abundantly in the brain. For the first time, the formation and biological actions of these various classes of reactive cyclopentenone eicosanoids are reviewed, with emphasis on their potential roles in neurodegeneration. The accumulating evidence suggests that the formation of cyclopentenone eicosanoids in the brain may represent a novel pathogenic mechanism, which contributes to many neurodegenerative conditions.
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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.