Roles of gut microbiota metabolites in the pathogenesis of migraine
- 1Jining Medical University , ,
- 2Department of Neurology, Affiliated Hospital of Jining Medical University , ,
- 3Department of Gastroenterology, Affiliated Hospital of Jining Medical University , ,
Abstract
Migraine is one of the most common neurological disorders, with a complex and incompletely understood pathogenesis. Recent studies have implicated the gut-brain axis in migraine pathophysiology. The gut microbiota and microbiota-related metabolites may influence migraine-related processes through neural, immune, endocrine, and metabolic pathways. This review summarizes the potential roles of microbiota-derived metabolites in migraine through the gut-brain axis, with a focus on short-chain fatty acids (SCFAs), tryptophan (Trp)-related metabolites, and nitric oxide (NO)-related metabolic pathways, and their potential effects on neuroimmune signaling, intestinal barrier integrity, and trigeminovascular function. Current evidence suggests that gut dysbiosis and metabolic disturbances are associated with migraine and may modulate neuroinflammatory pathways and central sensitization; however, direct causal evidence in humans remains limited. Interventions targeting the gut microbiota or related metabolic pathways, including probiotics and dietary modifications, may represent potential adjunctive strategies, although current clinical evidence remains limited and heterogeneous.
Related
- Preliminary exploration of the pathogenesis of patent foramen ovale-related migraine and efficacy analysis of PFO closure
- Immune cells in the pathogenesis of abdominal aortic aneurysm: Roles, regulation and targeted interventions
- Identification of Genes Associated with Gut Microbiota Metabolites in Type 2 Diabetes Mellitus Complicated by Acute Cerebral Infarction Based on Bioinformatics and Mendelian Randomization
- Gut microbiota-derived phenylalanine metabolites exacerbate elderly-onset acute pancreatitis by promoting mitophagy and enhancing cell death
- Autophagy–Gut Microbiota–Epigenetic Interactions in Disease Pathogenesis: Focus on Neurodegenerative and Neuropsychiatric Disorders and Therapeutic Perspectives
BibTeX
@article{shi2026roles,
title = {{Roles of gut microbiota metabolites in the pathogenesis of migraine}},
author = {Yadi Shi and Yifan Cao and Ziyu Zhang and Ruolin Li and Guangxi Zhou and Peng Xu},
journal = {Frontiers in medicine},
year = {2026},
month = oct,
doi = {10.3389/fmed.2026.1949484},
url = {https://europepmc.org/article/PMC/PMC13720901},
note = {CC BY},
}
RIS
TY - JOUR
TI - Roles of gut microbiota metabolites in the pathogenesis of migraine
AU - Yadi Shi
AU - Yifan Cao
AU - Ziyu Zhang
AU - Ruolin Li
AU - Guangxi Zhou
AU - Peng Xu
PY - 2026
DA - 2026/10/16
JO - Frontiers in medicine
DO - 10.3389/fmed.2026.1949484
UR - https://europepmc.org/article/PMC/PMC13720901
AB - Migraine is one of the most common neurological disorders, with a complex and incompletely understood pathogenesis. Recent studies have implicated the gut-brain axis in migraine pathophysiology. The gut microbiota and microbiota-related metabolites may influence migraine-related processes through neural, immune, endocrine, and metabolic pathways. This review summarizes the potential roles of microbiota-derived metabolites in migraine through the gut-brain axis, with a focus on short-chain fatty acids (SCFAs), tryptophan (Trp)-related metabolites, and nitric oxide (NO)-related metabolic pathways, and their potential effects on neuroimmune signaling, intestinal barrier integrity, and trigeminovascular function. Current evidence suggests that gut dysbiosis and metabolic disturbances are associated with migraine and may modulate neuroinflammatory pathways and central sensitization; however, direct causal evidence in humans remains limited. Interventions targeting the gut microbiota or related metabolic pathways, including probiotics and dietary modifications, may represent potential adjunctive strategies, although current clinical evidence remains limited and heterogeneous.
SN - 2296-858X
ER -