ReviewFrontiers in neuroscience2015
Rational modulation of the innate immune system for neuroprotection in ischemic stroke.
Review in Frontiers in neuroscience, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 120 papers.
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Who cites it
120 citing papers in PubMed, 206 citations in OpenAlex.
- Serendipitous Discovery of Short Peptides Dimethylammonium Salt Promoting Neural Differentiation.Journal of peptide science : an official publication of the European Peptide Society · 2026Article
- Sugiol Alleviates Cerebral Ischemia/Reperfusion Injury in the Early Phase Involving the LRRK2/NF-κB Pathway.Cell biochemistry and biophysics · 2026Article
- Targeting the interactions between neutrophils and microglia: a novel strategy for anti-inflammatory treatment of stroke.Acta pharmacologica Sinica · 2026Review
- Article
- Expression Patterns of T-Cell Intracellular Antigen 1 in Neurodegenerative Disorders and Stroke.International journal of molecular sciences · 2026Review
- Does Neuroglobin Protect Against Stroke? Insights Into the Role of Neurovascular Unit Cells.Cellular and molecular neurobiology · 2026Review
- Mild Subcortical Stroke Induces Widespread Chronic Reactive Astrogliosis That Is Largely Unaffected by Microglia and Age.ASN neuro · 2026Article
- Insights gained from single-cell sequencing analysis of ischemic stroke.Frontiers in cell and developmental biology · 2026Review
- Immunological and Inflammatory Biomarkers in the Prognosis, Prevention, and Treatment of Ischemic Stroke: A Review of a Decade of Advancement.International journal of molecular sciences · 2025Review
- Neutrophils induce astrocytic AQP4 expression via IL-1α and TNF, contributing to cerebral oedema in ischaemic stroke rats.Scientific reports · 2025Article
- Immune-mediated blood-brain barrier disruption after ischemic stroke: mechanisms and therapeutic targets.Frontiers in immunology · 2025Review
- Review
- Interleukin-4 prevents increased endothelial permeability by inducing pericyte survival and modulating microglial responses in diabetic retinopathy.Frontiers in endocrinology · 2025Article
- Identification of a potential miRNA-mRNA regulatory network for ischemic stroke by using bioinformatics methods: a retrospective study based on the Gene Expression Omnibus database.Frontiers in immunology · 2025Article
- The Neuroprotection of 1,2,4-Triazole Derivative by Inhibiting Inflammation and Protecting BBB Integrity in Acute Ischemic Stroke.CNS neuroscience & therapeutics · 2024Article
- Benserazide is neuroprotective and improves functional recovery after experimental ischemic stroke by altering the immune response.Scientific reports · 2024Article
- Article
- The Role of Neutrophils in Multiple Sclerosis and Ischemic Stroke.Brain sciences · 2024Review
- Identification of hypoxia- and immune-related biomarkers in patients with ischemic stroke.Heliyon · 2024Article
- Identification of ribosome biogenesis genes and subgroups in ischaemic stroke.Frontiers in immunology · 2024Article
60 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
9 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The innate immune system plays a dualistic role in the evolution of ischemic brain damage and has also been implicated in ischemic tolerance produced by different conditioning stimuli. Early after ischemia, perivascular astrocytes release cytokines and activate metalloproteases (MMPs) that contribute to blood-brain barrier (BBB) disruption and vasogenic oedema; whereas at later stages, they provide extracellular glutamate uptake, BBB regeneration and neurotrophic factors release. Similarly, early activation of microglia contributes to ischemic brain injury via the production of inflammatory cytokines, including tumor necrosis factor (TNF) and interleukin (IL)-1, reactive oxygen and nitrogen species and proteases. Nevertheless, microglia also contributes to the resolution of inflammation, by releasing IL-10 and tumor growth factor (TGF)-β, and to the late reparative processes by phagocytic activity and growth factors production. Indeed, after ischemia, microglia/macrophages differentiate toward several phenotypes: the M1 pro-inflammatory phenotype is classically activated via toll-like receptors or interferon-γ, whereas M2 phenotypes are alternatively activated by regulatory mediators, such as ILs 4, 10, 13, or TGF-β. Thus, immune cells exert a dualistic role on the evolution of ischemic brain damage, since the classic phenotypes promote injury, whereas alternatively activated M2 macrophages or N2 neutrophils prompt tissue remodeling and repair. Moreover, a subdued activation of the immune system has been involved in ischemic tolerance, since different preconditioning stimuli act via modulation of inflammatory mediators, including toll-like receptors and cytokine signaling pathways. This further underscores that the immuno-modulatory approach for the treatment of ischemic stroke should be aimed at blocking the detrimental effects, while promoting the beneficial responses of the immune reaction.
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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.