Gut Microbiota and Stroke: New Insights into the Gut–Brain–Vascular Axis

Jan 31, 2026Current atherosclerosis reports

Gut Bacteria and Stroke: New Understanding of the Gut-Brain-Blood Vessel Connection

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Circadian Biology on OpenScience ↗PubMed ↗DOI ↗

Abstract

Specific profiles of gut microbiota are associated with stroke severity and clinical outcomes.

Dysfunction of the gut barrier and endotoxin translocation may induce low-grade systemic inflammation, a common mechanism for cerebrovascular events and atherosclerosis.
Microbial metabolites such as trimethylamine-N-oxide (TMAO), short-chain fatty acids (SCFAs), and bile acids (BAs) could modulate endothelial function and blood-brain barrier (BBB) permeability.
Elevated syndecan-1 (SDC1) may indicate endothelial injury and serve as a potential stroke biomarker.
Altered tryptophan metabolism via the kynurenine pathway is linked to neuroinflammation and connects gut dysbiosis to cerebrovascular disease.
Preventing dysbiosis may reduce stroke risk, while post-stroke microbiota modulation could improve recovery.

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PURPOSE OF REVIEW: Recent advances have underscored the importance of interactions between the gut microbiota, vascular system and brain in stroke pathogenesis. This review introduces the conceptual framework of the gut-brain-vascular axis and summarizes evidence on how microbiota affects neurovascular integrity and stroke outcomes via intricate immunological, metabolic and endothelial mechanisms.

RECENT FINDINGS: Recent clinical and epidemiological studies have demonstrated that specific profiles of gut microbiota are associated with stroke severity and clinical outcomes. Dysfunction of the gut barrier integrity and the translocation of endotoxins can induce low-grade systemic inflammation, which is a common mechanism underlying both cerebrovascular events and atherogenesis. Furthermore, microbial metabolites such as trimethylamine-N-oxide (TMAO), short-chain fatty acids (SCFAs) and bile acids (BAs) have been shown to modulate endothelial function, platelet hyperactivation and blood-brain barrier (BBB) permeability. Advances in BBB modelling reveal how microbial signals contribute to neurovascular dysfunction. Glycocalyx disruption, marked by elevated syndecan-1 (SDC1), reflects endothelial injury and could be used as a stroke biomarker. Furthermore, altered tryptophan metabolism via the kynurenine pathway is a contributing factor to neuroinflammation, thereby establishing a link between gut dysbiosis and cerebrovascular pathology. Emerging evidence on the gut-brain-vascular axis indicates that preventing dysbiosis may reduce stroke risk, while post-stroke modulation of the microbiota could enhance recovery. The gut-brain-vascular axis provides a novel and integrative model linking gut microbiota disfunction to neurovascular and atherosclerotic disease. Understanding these interconnected pathways may inform future approaches to risk stratification and cerebrovascular disease prevention and treatment.

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Gut Microbiota and Stroke: New Insights into the Gut–Brain–Vascular Axis

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