ReviewFrontiers in neuroscience2026
The bridging role of gut microbiota-derived metabolites in neuropathic pain comorbid with anxiety.
Review in Frontiers in neuroscience, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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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.
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Who cites it
1 citing paper in PubMed.
- Psyllium and Glucomannan as Viscous Fiber Modulators of the Gut-Microbiome-Incretin Axis: Molecular Links to Metabolic Inflammation, Barrier Function, and GLP-1 Receptor Agonist Therapy.International journal of molecular sciences · 2026Review
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Authors and funding
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Abstract
Neuropathic pain (NP) is a chronic pain condition caused by damage or disease of the somatosensory system and often forms a comorbid state with anxiety, severely affecting patients' quality of life. The occurrence of this comorbidity involves the interplay of multiple mechanisms, including neuroinflammation, metabolic abnormalities, the hypothalamic-pituitary-adrenal (HPA) axis dysregulation, and imbalances in central neurotransmitter systems. In recent years, research on the mechanisms by which gut microbiota-derived metabolites regulate NP and anxiety via the "gut-brain axis" has garnered increasing attention. Among the numerous gut microbiota-derived metabolites, lipopolysaccharide (LPS), short-chain fatty acids (SCFAs), bile acids (BAs), serotonin (5-HT), and γ-aminobutyric acid (GABA) are considered key signaling molecules. They collectively participate in the pathological process of NP-anxiety comorbidity by regulating immune responses, metabolic pathways, and neural pathways. This review focuses on these five metabolites, analyzing the bridging role of their functional abnormalities in this comorbidity and future directions in this field.
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Registered trials
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