ArticlePPAR research2008
Therapeutic Potential of PPARγ Activation in Stroke.
Article in PPAR research, 2008. 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.
- Role of transcription factors, noncoding RNAs, epitranscriptomics, and epigenetics in post-ischemic neuroinflammation.Journal of neurochemistry · 2024Review
- Exposure to Environmental Toxins: Potential Implications for Stroke Risk via the Gut- and Lung-Brain Axis.Cells · 2024Review
- Aspects of xenobiotics and their receptors in stroke.Neuroprotection (Chichester, England) · 2023Review
- Microglial Inflammatory-Metabolic Pathways and Their Potential Therapeutic Implication in Major Depressive Disorder.Frontiers in psychiatry · 2022Review
- Peroxisome Proliferator-Activated Receptor-Gamma (PPAR-ɣ): Molecular Effects and Its Importance as a Novel Therapeutic Target for Cerebral Ischemic Injury.Neurochemical research · 2021Review
- Optimisation of a PC12 cell-based in vitro stroke model for screening neuroprotective agents.Scientific reports · 2021Article
- Post-Ischaemic Immunological Response in the Brain: Targeting Microglia in Ischaemic Stroke Therapy.Brain sciences · 2020Review
- Pleiotropic role of PPARγ in intracerebral hemorrhage: an intricate system involving Nrf2, RXR, and NF-κB.CNS neuroscience & therapeutics · 2015Review
- PPARγ agonists improve survival and neurocognitive outcomes in experimental cerebral malaria and induce neuroprotective pathways in human malaria.PLoS pathogens · 2014Article
- Prevention of JNK phosphorylation as a mechanism for rosiglitazone in neuroprotection after transient cerebral ischemia: activation of dual specificity phosphatase.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2013Article
- The Case for the Use of PPARγ Agonists as an Adjunctive Therapy for Cerebral Malaria.PPAR research · 2012Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
1 author.
Funding
Abstract
Stroke (focal cerebral ischemia) is a leading cause of death and disability among adult population. Many pathological events including inflammation and oxidative stress during the acute period contributes to the secondary neuronal death leading the neurological dysfunction after stroke. Transcriptional regulation of genes that promote these pathophysiological mechanisms can be an effective strategy to minimize the poststroke neuronal death. Peroxisome proliferator-activated receptors (PPARs) are ligand-activated transcription factors known to be upstream to many inflammatory and antioxidant genes. The goal of this review is to discuss the therapeutic potential and putative mechanisms of neuroprotection following PPAR activation after stroke.
Identifiers
What OpenQuestion 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 OpenQuestion graph.