ReviewInternational journal of molecular sciences2022
Polarization of Microglia and Its Therapeutic Potential in Sepsis.
Review in International journal of molecular sciences, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 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
18 citing papers in PubMed.
- Encephalopathy: Cause, Pathogenesis, and Treatment.MedComm · 2026Review
- Melatonin Mitigates Central Sensitization and Nociplastic Pain in Spinal Cord and Dorsal Root Ganglia of FM Rat Model: Modulation of SIRT1/PGC-1α/MAPK/NF-κB Signaling.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2026Article
- A Lipid Road to Neuroimmunology: Fatty Acids Linking Immune and Nervous Systems.Neuroimmunomodulation · 2026Review
- Glial Cells as Central Players in Neuroinflammation and Neuronal Damage Caused by Bacterial Pneumonia.Neuroimmunomodulation · 2026Review
- Engineering a targeted daphnetin delivery system to enhance spinal cord injury treatment effectiveness.Materials today. Bio · 2025Article
- Interleukin-37 modulates microglial phenotype and inhibits inflammatory response via the MyD88/NF-κB pathway in lipopolysaccharide-induced neuroinflammation.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2025Article
- PLGA nanoparticle-mediated anti-inflammatory gene delivery for the treatment of neuropathic pain.Nanomedicine (London, England) · 2025Article
- Research progress on the interaction between multiple organ-brain axes and perioperative neurocognitive disorders: a narrative review.Frontiers in aging neuroscience · 2025Review
- The Modulation of Neuroimmune Responses in Peripheral Inflammation.Journal of inflammation research · 2025Review
- p65 enhanced METTL3-mediated mCentral-European journal of immunology · 2025Article
- ACE2 Rescues Sepsis-Associated Encephalopathy by Reducing Inflammation, Oxidative Stress, and Neuronal Apoptosis via the Nrf2/Sestrin2 Signaling Pathway.Molecular neurobiology · 2024Article
- Sepsis-associated encephalopathy: Autophagy and miRNAs regulate microglial activation.Physiological reports · 2024Review
- Evaluating Nutritional Risk Factors for Delirium in Intensive-Care-Unit Patients: Present Insights and Prospects for Future Research.Clinics and practice · 2023Review
- Low-dose PLX5622 treatment prevents neuroinflammatory and neurocognitive sequelae after sepsis.Journal of neuroinflammation · 2023Article
- Regulation of oxygen-glucose deprivation/reperfusion-induced inflammatory responses and M1-M2 phenotype switch of BV2 microglia by lobetyolin.Metabolic brain disease · 2023Article
- Article
- Sepsis-Induced Brain Dysfunction: Pathogenesis, Diagnosis, and Treatment.Oxidative medicine and cellular longevity · 2022Review
- Central role of microglia in sepsis-associated encephalopathy: From mechanism to therapy.Frontiers in immunology · 2022Review
Corrections and comments
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Authors and funding
3 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Sepsis is a life-threatening organ dysfunction caused by a dysregulated host response to infection, leaving the inflammation process without a proper resolution, leading to tissue damage and possibly sequelae. The central nervous system (CNS) is one of the first regions affected by the peripheral inflammation caused by sepsis, exposing the neurons to an environment of oxidative stress, triggering neuronal dysfunction and apoptosis. Sepsis-associated encephalopathy (SAE) is the most frequent sepsis-associated organ dysfunction, with symptoms such as deliriums, seizures, and coma, linked to increased mortality, morbidity, and cognitive disability. However, the current therapy does not avoid those patients' symptoms, evidencing the search for a more optimal approach. Herein we focus on microglia as a prominent therapeutic target due to its multiple functions maintaining CNS homeostasis and its polarizing capabilities, stimulating and resolving neuroinflammation depending on the stimuli. Microglia polarization is a target of multiple studies involving nerve cell preservation in diseases caused or aggravated by neuroinflammation, but in sepsis, its therapeutic potential is overlooked. We highlight the peroxisome proliferator-activated receptor gamma (PPARγ) neuroprotective properties, its role in microglia polarization and inflammation resolution, and the interaction with nuclear factor-κB (NF-κB) and mitogen-activated kinases (MAPK), making PPARγ a molecular target for sepsis-related studies to come.
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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.