ReviewInternational journal of molecular sciences2020
A Fatal Alliance between Microglia, Inflammasomes, and Central Pain.
Review in International journal of molecular sciences, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
15 citing papers in PubMed, 29 citations in OpenAlex.
- Repurposed Systemic Pharmacologic Agents in Chronic Pain: Emerging Mechanistic and Clinical Insights.Journal of clinical medicine · 2026Review
- Microglia-mediated BLA glutamatergic neuronal hyperactivity in the BLA-ACC pathway contributes to stress-induced visceral hypersensitivity and anxiety in rats.Molecular medicine (Cambridge, Mass.) · 2025Article
- Review
- Mesenchymal stem cells as a therapeutic strategy to combat oxidative stress-mediated neuropathic pain.BioImpacts : BI · 2025Review
- NLRP3 Inflammasome Inhibitors for Antiepileptogenic Drug Discovery and Development.International journal of molecular sciences · 2024Review
- Netrin-1 Promotes M2 Type Activation and Inhibits Pyroptosis of Microglial Cells by Depressing RAC1/Nf-?B Pathway to Alleviate Inflammatory Pain.Physiological research · 2024Article
- Involvement of microglial P2X7 receptor in pain modulation.CNS neuroscience & therapeutics · 2024Review
- Microglia role in the pain phenomenon.Revista da Associacao Medica Brasileira (1992) · 2023Article
- Magnetic Resonance Images, Pathological Features of Thrombus, and Expression of NLRP Inflammasome in Patients with Acute Ischemic Stroke.Contrast media & molecular imaging · 2022Article
- Intrathecal Administration of an Anti-nociceptive Non-CpG Oligodeoxynucleotide Reduces Glial Activation and Central Sensitization.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2021Article
- Inflammasome Signaling Regulates the Microbial-Neuroimmune Axis and Visceral Pain in Mice.International journal of molecular sciences · 2021Article
- Ethyl Pyruvate Attenuates Microglial NLRP3 Inflammasome Activation via Inhibition of HMGB1/NF-κB/miR-223 Signaling.Antioxidants (Basel, Switzerland) · 2021Article
- The IL33 receptor ST2 contributes to mechanical hypersensitivity in mice with neuropathic pain.Molecular brain · 2021Article
- DOK3 is involved in microglial cell activation in neuropathic pain by interacting with GPR84.Aging · 2020Article
- COVID-19: Pain Management in Patients with SARS-CoV-2 Infection-Molecular Mechanisms, Challenges, and Perspectives.Brain sciences · 2020Article
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
Microglia are the resident immune cells in the CNS, which survey the brain parenchyma for pathogens, initiate inflammatory responses, secrete inflammatory mediators, and phagocyte debris. Besides, they play a role in the regulation of brain ion homeostasis and in pruning synaptic contacts and thereby modulating neural networks. More recent work shows that microglia are embedded in brain response related to stress phenomena, the development of major depressive disorders, and pain-associated neural processing. The microglia phenotype varies between activated-toxic-neuroinflammatory to non-activated-protective-tissue remodeling, depending on the challenges and regulatory signals. Increased inflammatory reactions result from brain damage, such as stroke, encephalitis, as well as chronic dysfunctions, including stress and pain. The dimension of damage/toxic stimuli defines the amplitude of inflammation, ranging from an on-off event to low but continuous simmering to uncontrollable. Pain, either acute or chronic, involves inflammasome activation at the point of origin, the different relay stations, and the sensory and processing cortical areas. This short review aimed at identifying a sinister role of the microglia-inflammasome platform for the development and perpetuation of acute and chronic central pain and its association with changes in CNS physiology.
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What OpenQuestion holds
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.