ReviewMolecular neurobiology2025
Gut Microbiota: A Modulator and Therapeutic Target for Chronic Pain.
Review in Molecular neurobiology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 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
7 citing papers in PubMed.
- Comorbidity Mechanism and Management of Chronic Low Back Pain and Major Depressive Disorder: From Neural Circuit Remodeling to Precision Medicine.Brain and behavior · 2026Review
- Gut-ocular surface axis in dry eye disease: phenotype-specific mechanisms, evidence, and microbiome-targeted interventions.Frontiers in cellular and infection microbiology · 2026Review
- The role of the gut microbiota in the development of rheumatic diseases: a focus on fibromyalgia.Frontiers in immunology · 2026Review
- Impact of antibiotic-induced gut microbiota modulation on morphine analgesia, tolerance, withdrawal, and neurophysiological changes in mice.Scientific reports · 2025Article
- State of the "Art" in Precision Health Symptom Science Research.Seminars in oncology nursing · 2025Review
- Neuromodulation in Chronic Migraine: Evidence and Recommendations from the GRADE Framework.Advances in therapy · 2025Review
- Emerging role of macrophages in neuropathic pain.Journal of orthopaedic translation · 2025Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Chronic pain is a prevalent condition, impacting nearly one-fifth of the global population. Despite the availability of various clinical treatments, each comes with inherent limitations, and few offer a complete cure, resulting in a significant social and economic burden. Therefore, it is important to determine the pathogenesis and causes of chronic pain. Numerous studies have shown a close link between the intestinal microflora and chronic pain. The gut microbiota can exert their effects on chronic pain through both central and peripheral mechanisms and is able to communicate with the brain through its own components or metabolites. They also can regulate chronic pain by affecting pro- and anti-inflammatory cells. This review is aimed at reviewing the connection between gut flora and different types of chronic pain, including visceral pain, neuropathic pain, inflammatory pain, musculoskeletal pain, migraine, and chronic cancer pain; exploring the central and peripheral mechanisms of the influence of gut flora on chronic pain; and attempting to provide novel treatment options for chronic pain, that is, the gut microbiota can be regulated by probiotics, fecal microbial transplantation, and natural products to treat chronic pain. By examining the intricate relationship between gut flora and chronic pain, the review sought to pave the way for new treatment strategies that target the gut microbiota, offering hope for more effective pain management.
Indexed as
Identifiers
39652283What 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.