ReviewMolecular biology reports2025
Beyond inflammation: a comprehensive microglial regulation model in chronic pain.
Review in Molecular biology reports, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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
2 citing papers in PubMed.
- Article
- TNFR-CD3-engineered regulatory T cells attenuate neuroinflammation and neuropathic pain.Immunologic research · 2026Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors.
Funding
Abstract
Chronic pain has emerged as a disorder of persistent neuroimmune dysregulation, with microglia playing a pivotal role in shaping maladaptive plasticity. Beyond classical inflammatory pathways, recent discoveries highlight microglial involvement in epigenetic remodeling, metabolic reprogramming, and synaptic modulation. These multidimensional processes sustain microglial activation and promote central sensitization, even in the absence of ongoing peripheral injury. This review proposes a comprehensive framework for understanding microglial regulation in chronic pain, emphasizing the failure of immune tolerance, aberrant neuron-glia signaling, and the emergence of disease-perpetuating microglial states. We further discuss therapeutic strategies aimed at selectively targeting microglial phenotypes, including HDAC inhibitors, metabolic modulators, and pathway-specific antagonists. By integrating mechanistic depth with translational insights, this review reframes microglia not only as inflammatory mediators, but as dynamic regulators whose dysregulation underlies pain chronification.
Indexed as
Identifiers
40952595What 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.