ReviewSeminars in immunopathology2019
Resolution of neuroinflammation: mechanisms and potential therapeutic option.
Review in Seminars in immunopathology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 50 papers, 1 of them a synthesis 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
50 citing papers in PubMed, 1 synthesis or guideline pooled it, 86 citations in OpenAlex.
- A systematic review of alterations in sensorimotor networks following stroke: implications for integration and functional outcomes across recovery stages.Frontiers in neurology · 2025Pooled it
- Regulatory T cells in stroke inflammation: Therapeutic perspectives.Neural regeneration research · 2026Article
- Targeting the interactions between neutrophils and microglia: a novel strategy for anti-inflammatory treatment of stroke.Acta pharmacologica Sinica · 2026Review
- Neuroinflammation: Mechanisms, Dual Roles, and Therapeutic Strategies in Neurological Disorders.Current issues in molecular biology · 2025Review
- TRIM14 Inhibition Suppresses Microglial Polarization and Pyroptosis Through the NF-κB/NLRP3 Pathway to Enhance Spinal Cord Injury Repair.Mediators of inflammation · 2025Article
- Selective neuronal expression of progranulin is sufficient to provide neuroprotective and anti-inflammatory effects after traumatic brain injury.Journal of neuroinflammation · 2024Article
- Translational Medicine in Acute Ischemic Stroke and Traumatic Brain Injury-NeuroAiD Trials, from Traditional Beliefs to Evidence-Based Therapy.Biomolecules · 2024Review
- Pannexin1 Channel-Mediated Inflammation in Acute Ischemic Stroke.Aging and disease · 2024Review
- Neuroinflammation and Epilepsy: From Pathophysiology to Therapies Based on Repurposing Drugs.International journal of molecular sciences · 2024Review
- Erythropoietin alleviates astrocyte pyroptosis by targeting the miR-325-3p/Gsdmd axis in rat spinal cord injury.Inflammopharmacology · 2024Article
- Downregulation of Circular RNA Gla Reduced Astrocyte Inflammatory Status by Regulating miR-488/MEKK1 Levels and Promoted Functional Recovery After Spinal Cord Injury.Journal of inflammation research · 2024Article
- Fingerprint of Circulating Immunocytes as Biomarkers for the Prognosis of Brain Inflammation and Neuronal Injury after Cardiac Arrest.ACS chemical neuroscience · 2023Article
- Stimulation of the Pro-Resolving Receptor Fpr2 Reverses Inflammatory Microglial Activity by Suppressing NFκB Activity.International journal of molecular sciences · 2023Article
- Article
- Polyunsaturated Fatty Acids: Conversion to Lipid Mediators, Roles in Inflammatory Diseases and Dietary Sources.International journal of molecular sciences · 2023Review
- IL1RAP Knockdown in LPS-Stimulated Normal Human Astrocytes Suppresses LPS-Induced Reactive Astrogliosis and Promotes Neuronal Cell Proliferation.Neurochemical research · 2023Article
- The Role of Probiotics and Their Metabolites in the Treatment of Depression.Molecules (Basel, Switzerland) · 2023Review
- Transcriptional changes in the rat brain induced by repetitive transcranial magnetic stimulation.Frontiers in human neuroscience · 2023Article
- Fatty Acid-DerivedNutrients · 2022Article
- Cytokine changes in cerebrospinal fluid following vascular surgery on the thoracic aorta.Scientific reports · 2022Article
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 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The central nervous system (CNS) is comprised by an elaborate neural network that is under constant surveillance by tissue-intrinsic factors for maintenance of its homeostasis. Invading pathogens or sterile injuries might compromise vitally the CNS integrity and function. A prompt anti-inflammatory response is therefore essential to contain and repair the local tissue damage. Although the origin of the insults might be different, the principles of tissue backlashes, however, share striking similarities. CNS-resident cells, such as microglia and astrocytes, together with peripheral immune cells orchestrate an array of events that aim to functional restoration. If the acute inflammatory event remains unresolved, it becomes toxic leading to progressive CNS degeneration. Therefore, the cellular, molecular, and biochemical processes that regulate inflammation need to be on a fine balance with the intrinsic CNS repair mechanisms that influence tissue healing. The purpose of this review is to highlight aspects that facilitate the resolution of CNS inflammation, promote tissue repair, and functional recovery after acute injury and infection that could potentially contribute as therapeutic interventions.
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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.