ReviewNeuroscience letters2016
Epigenetic modulation of gene expression governs the brain's response to injury.
Review in Neuroscience letters, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 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.
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Who cites it
7 citing papers in PubMed.
- The Role of the lncRNA MALAT1 in Neuroprotection against Hypoxic/Ischemic Injury.Biomolecules · 2022Review
- HDAC1 Expression, Histone Deacetylation, and Protective Role of Sodium Valproate in the Rat Dorsal Root Ganglia After Sciatic Nerve Transection.Molecular neurobiology · 2021Article
- Histone acetylation and DNA methylation in ischemia/reperfusion injury.Clinical science (London, England : 1979) · 2019Review
- Brain Functional Reserve in the Context of Neuroplasticity after Stroke.Neural plasticity · 2019Review
- Neutrophil-Related Oxidants Drive Heart and Brain Remodeling After Ischemia/Reperfusion Injury.Frontiers in physiology · 2019Review
- The vagal ganglia transcriptome identifies candidate therapeutics for airway hyperreactivity.American journal of physiology. Lung cellular and molecular physiology · 2018Article
- Adaptive Plasticity in the Retina: Protection Against Acute Injury and Neurodegenerative Disease by Conditioning Stimuli.Conditioning medicine · 2018Article
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
Mild stress from ischemia, seizure, hypothermia, or infection can produce a transient neuroprotected state in the brain. In the neuroprotected state, the brain responds differently to a severe stress and sustains less injury. At the genomic level, the response of the neuroprotected brain to a severe stress is characterized by widespread differential regulation of genes with diverse functions. This reprogramming of gene expression observed in the neuroprotected brain in response to a stress is consistent with an epigenetic model of regulation mediated by changes in DNA methylation and histone modification. Here, we summarize our evolving understanding of the molecular basis for endogenous neuroprotection and review recent findings that implicate DNA methylation and protein mediators of histone modification as epigenetic regulators of the brain's response to injury.
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Registered trials
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