ReviewFrontiers in pharmacology2020
Microglia: A Potential Therapeutic Target for Sepsis-Associated Encephalopathy and Sepsis-Associated Chronic Pain.
Review in Frontiers in pharmacology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 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
29 citing papers in PubMed, 2 syntheses or guidelines pooled it, 54 citations in OpenAlex.
- New trends and hotspots in Sepsis-associated encephalopathy research: a bibliometric and visualization analysis.Frontiers in aging neuroscience · 2026Pooled it
- The core role of central nervous system in sepsis-related organ damage.Frontiers in immunology · 2025Pooled it
- INPP5D Upregulation by Minocycline Mitigates Sepsis-Associated Neuroinflammation and Neuronal Dysfunction Via Microglial Autophagy and Antioxidant Pathways.Inflammation · 2026Article
- Pharmacological inhibition of the cGAS-STING pathway suppresses microglia pyroptosis in sepsis-associated encephalopathy.Journal of neuroinflammation · 2025Article
- Association between advanced lung cancer inflammation index and all-cause mortality in critically ill patients with sepsis: analysis of the MIMIC-IV database.Scientific reports · 2025Article
- Role of GLP‑1 receptor agonists in sepsis and their therapeutic potential in sepsis‑induced muscle atrophy (Review).International journal of molecular medicine · 2025Review
- Decoding pain chronification: mechanisms of the acute-to-chronic transition.Frontiers in molecular neuroscience · 2025Review
- Glutathione metabolism as a key regulator of oxidative hippocampal injury in sepsis-associated encephalopathy: an integrated proteomics and metabolomics study.Frontiers in neuroscience · 2025Article
- The Biological Changes of Synaptic Plasticity in the Pathological Process of Sepsis-associated Encephalopathy.Current neuropharmacology · 2025Review
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- CD137L Inhibition Ameliorates Hippocampal Neuroinflammation and Behavioral Deficits in a Mouse Model of Sepsis-Associated Encephalopathy.Neuromolecular medicine · 2023Article
- Resolvin D1 attenuates depressive-like behavior in LPS-challenged mice by promoting microglial autophagy.Inflammopharmacology · 2023Article
- Maresin1 Ameliorates Sepsis-Induced Microglial Neuritis Induced through Blocking TLR4-NF-κ B-NLRP3 Signaling Pathway.Journal of personalized medicine · 2023Article
- ß1-adrenergic blockers preserve neuromuscular function by inhibiting the production of extracellular traps during systemic inflammation in mice.Frontiers in immunology · 2023Article
- Application background and mechanism of short-chain fatty acids in sepsis-associated encephalopathy.Frontiers in cellular and infection microbiology · 2023Review
- Review of Neurofilaments as Biomarkers in Sepsis-Associated Encephalopathy.Journal of inflammation research · 2023Review
- Electroacupuncture Alleviates Neuroinflammation by Inhibiting the HMGB1 Signaling Pathway in Rats with Sepsis-Associated Encephalopathy.Brain sciences · 2022Article
- Polarization of Microglia and Its Therapeutic Potential in Sepsis.International journal of molecular sciences · 2022Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Neurological dysfunction, one of the severe manifestations of sepsis in patients, is closely related to increased mortality and long-term complications in intensive care units, including sepsis-associated encephalopathy (SAE) and chronic pain. The underlying mechanisms of these sepsis-induced neurological dysfunctions are elusive. However, it has been well established that microglia, the dominant resident immune cell in the central nervous system, play essential roles in the initiation and development of SAE and chronic pain. Microglia can be activated by inflammatory mediators, adjacent cells and neurotransmitters in the acute phase of sepsis and then induce neuronal dysfunction in the brain. With the spotlight focused on the relationship between microglia and sepsis, a deeper understanding of microglia in SAE and chronic pain can be achieved. More importantly, clarifying the mechanisms of sepsis-associated signaling pathways in microglia would shed new light on treatment strategies for SAE and chronic pain.
Indexed as
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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.