ArticleMedComm2024
Inhibition of 15-hydroxyprostaglandin dehydrogenase protects neurons from ferroptosis in ischemic stroke.
Article in MedComm, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
11 citing papers in PubMed, 11 citations in OpenAlex.
- Targeting prostaglandin catabolism via topical nanotherapy rescues vision in ischemic optic neuropathy.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2026Article
- Prostaglandins: Key players in immunomodulation of the nervous system.Neural regeneration research · 2026Article
- Inhibiting 15-PGDH restores redox homeostasis and confers neuroprotection in Parkinson's disease.Redox biology · 2026Article
- Targeting Ferroptosis and Necroptosis to Treat Stroke.Neurochemical research · 2026Review
- Insights into the potential pathogenesis and therapeutic implications of ferroptosis in brain microvascular endothelial cells during stroke.Frontiers in immunology · 2026Review
- Phylloquinone Attenuates Oxygen-Glucose Deprivation-induced Neuronal Injury by Inhibiting Ferroptosis via the xCT/GPX4 Pathway.Neurochemical research · 2025Article
- Inhibiting 15-PGDH blocks blood-brain barrier deterioration and protects mice from Alzheimer's disease and traumatic brain injury.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Bioinformatics analysis of comorbid mechanisms between ischemic stroke and end stage renal disease.Scientific reports · 2025Article
- p23 protects against ferroptosis of brain microvascular endothelial cells in ischemic stroke.International journal of molecular medicine · 2025Article
- Atorvastatin inhibits ischemia‒reperfusion-associated renal tubular cell ferroptosis by blocking the PGE2/EP4 signaling pathway.In vitro cellular & developmental biology. Animal · 2025Article
- Inhibition of 15-hydroxyprostaglandin dehydrogenase protects neurons from ferroptosis in ischemic stroke.MedComm · 2024Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Ischemic stroke is an acute serious cerebrovascular disease with high mortality and disability. Ferroptosis is an important regulated cell death (RCD) in ischemic stroke. 15-Hydroxyprostaglandin dehydrogenase (15-PGDH), a degrading enzyme of prostaglandin E2 (PGE2), is shown to regulate RCD such as autophagy and apoptosis. The study aimed to determine whether 15-PGDH regulates ferroptosis and ischemic stroke, and further the exact mechanism. We demonstrated that overexpression of 15-PGDH in the brain tissues or primary cultured neurons significantly aggravated cerebral injury and neural ferroptosis in ischemic stroke. While inhibition of 15-PGDH significantly protected against cerebral injury and neural ferroptosis, which benefits arise from the activation of the PGE2/PGE2 receptor 4 (EP4) axis. While the impact of 15-PGDH was abolished with glutathione peroxidase 4 (GPX4) deficiency. Then, 15-PGDH inhibitor was found to promote the activation of cAMP-response element-binding protein (CREB) and nuclear factor kappa-B (NF-κB) via the PGE2/EP4 axis, subsequently transcriptionally upregulate the expression of GPX4. In summary, our study indicates that inhibition of 15-PGDH promotes the activation PGE2/EP4 axis, subsequently transcriptionally upregulates the expression of GPX4 via CREB and NF-κB, and then protects neurons from ferroptosis and alleviates the ischemic stroke. Therefore, 15-PGDH may be a potential therapeutic target for ischemic stroke.
Indexed as
Identifiers
What Socratic holds
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 Socratic graph.