What question did this study set out to answer?

The study aims to explore how gut microbiota dysfunction contributes to stress-related aortic dissection.

April 12, 2026Open Access

Gut microbiota dysfunction mediates stress-exacerbated aortic dissection via the bacteroides vulgatus-outer membrane vesicles-stearic acid-JNK/MAPK axis

Key Points

The study aims to explore how gut microbiota dysfunction contributes to stress-related aortic dissection.
Examined the role of B. vulgatus and its metabolites in aortic dissection.
Analyzed JNK/MAPK signaling pathways in vascular smooth muscle cells.
Investigated the therapeutic potential of restoring stearic acid levels.
Chronic stress reduced B. vulgatus abundance and stearic acid levels.
Decreased levels led to heightened JNK/MAPK signaling in vascular smooth muscle cells.
Restoring stearic acid inhibited this signaling pathway and slowed aortic dissection progression.

Abstract

CRS exacerbates the pathogenesis of AD by disrupting the gut microbiota, particularly by reducing the abundance of B. vulgatus and the levels of SA, which is a metabolite encapsulated in the OMVs of B. vulgatus. This leads to unchecked JNK/MAPK signaling, driving detrimental VSMC transformation. Restoration of SA inhibits this pathway and mitigates AD progression. Targeting the gut microbiota-B. vulgatus-SA axis presents a novel therapeutic strategy for stress-aggravated AD.

Gut microbiota dysfunction mediates stress-exacerbated aortic dissection via the bacteroides vulgatus-outer membrane vesicles-stearic acid-JNK/MAPK axis

Key Points

Abstract

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