ReviewProgress in neurobiology2016
Astrocytes, therapeutic targets for neuroprotection and neurorestoration in ischemic stroke.
Review in Progress in neurobiology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 338 papers, 2 of them syntheses that pooled it.
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
338 citing papers in PubMed, 2 syntheses or guidelines pooled it, 580 citations in OpenAlex.
- Pooled it
- Exosomes in pathogenesis, diagnosis, and therapy of ischemic stroke.Frontiers in bioengineering and biotechnology · 2022Pooled it
- The roles of microglia and astrocytes in inflammasomes and neurological disorders.Neural regeneration research · 2026Article
- Astrocytic Redox Homeostasis as a Metabolic Modulator of DNA Damage and Repair in the Ischemic Penumbra.Cells · 2026Review
- Astrocyte-derived IL-17A facilitates angiogenesis following ischemia-like injury via an IL-6-dependent STAT3-VEGF signaling cascade.Behavioral and brain functions : BBF · 2026Article
- Neuroinflammation-induced downregulation of RAB7 in murine astrocytes disrupts endo-lysosomal homeostasis and induces astrogliosis.Cell communication and signaling : CCS · 2026Article
- Physical crowding in 3D niche regulates neural stem cell differentiation via Cx43-mediated gap junction communication.iScience · 2026Article
- Article
- The rise of astrocytes: are they guardians or troublemakers of the brain disorder?Experimental & molecular medicine · 2026Review
- Expression Patterns of T-Cell Intracellular Antigen 1 in Neurodegenerative Disorders and Stroke.International journal of molecular sciences · 2026Review
- Targeting Reactive Astrocytes with Flavonoids to Alleviate Neuroinflammation and Promote Synaptic Function.Molecular neurobiology · 2026Review
- Targeting angiogenesis and white matter repair for enhanced functional recovery after acute ischemic stroke: A focus on the roles of glial cells.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2026Review
- The nitrate-nitrite-nitric oxide pathway of neuroinflammation and cognitive impairment in ischemic stroke.Frontiers in immunology · 2026Review
- METTL16 Promotes Cerebral Ischemia-Reperfusion Injury via mInternational journal of general medicine · 2026Article
- The mTOR/Akt pathway is involved in regulating astrocyte growth and GLT-1 expression during cerebral ischemia-reperfusion.PloS one · 2026Article
- The Mechanisms and Application Prospects of Astrocyte Reprogramming into Neurons in Central Nervous System Diseases.Current neuropharmacology · 2026Review
- Regulatory mechanisms and research progress of astrocytes in the neuro-endocrine-immune network.Frontiers in human neuroscience · 2026Review
- Lysine Demethylase 5B Alleviates Neuroinflammation in Ischemic Stroke by Repressing Steap4.Cell biochemistry and biophysics · 2025Article
- Melatonin Attenuates the Inflammatory Response of Astrocyte Following Ischemia Stroke through SIRT1/NF-κΒ Signaling Pathway.Molecular neurobiology · 2025Article
- Electroacupuncture Alleviates Cerebral Ischemia-Reperfusion Injury by Downregulating IL-17 A and Inhibiting Neurotoxic Astrocyte Activation.Neurochemical research · 2025Article
278 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 2 institutions in 1 country.
Funding
Abstract
Astrocytes are the most abundant cell type within the central nervous system. They play essential roles in maintaining normal brain function, as they are a critical structural and functional part of the tripartite synapses and the neurovascular unit, and communicate with neurons, oligodendrocytes and endothelial cells. After an ischemic stroke, astrocytes perform multiple functions both detrimental and beneficial, for neuronal survival during the acute phase. Aspects of the astrocytic inflammatory response to stroke may aggravate the ischemic lesion, but astrocytes also provide benefit for neuroprotection, by limiting lesion extension via anti-excitotoxicity effects and releasing neurotrophins. Similarly, during the late recovery phase after stroke, the glial scar may obstruct axonal regeneration and subsequently reduce the functional outcome; however, astrocytes also contribute to angiogenesis, neurogenesis, synaptogenesis, and axonal remodeling, and thereby promote neurological recovery. Thus, the pivotal involvement of astrocytes in normal brain function and responses to an ischemic lesion designates them as excellent therapeutic targets to improve functional outcome following stroke. In this review, we will focus on functions of astrocytes and astrocyte-mediated events during stroke and recovery. We will provide an overview of approaches on how to reduce the detrimental effects and amplify the beneficial effects of astrocytes on neuroprotection and on neurorestoration post stroke, which may lead to novel and clinically relevant therapies for stroke.
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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.