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Review
. 2024 Oct 26;10(21):e39865.
doi: 10.1016/j.heliyon.2024.e39865. eCollection 2024 Nov 15.

Roseburia intestinalis: A possible target for vascular calcification

Affiliations
Review

Roseburia intestinalis: A possible target for vascular calcification

Xinyun Pan et al. Heliyon. .

Abstract

With the advancement of metagenomics and metabolomics techniques, the crucial role of the gut microbiome in intestinal, cardiovascular, and metabolic disorders has been extensively explored. Vascular calcification (VC) is common in atherosclerosis, hypertension, diabetes mellitus, and chronic kidney disease. Moreover, it is a significant cause of cardiovascular diseases and mortality. Roseburia intestinalis, as a promising candidate for the next generation of probiotics, plays a substantial role in inhibiting the systemic inflammatory response and holds great potential in the treatment of intestinal diseases, cardiovascular diseases, and metabolic disorders. Its primary metabolite, butyrate, acts on specific receptors (GPR43, GPR41, GPR109a). It enters cells via transporters (MCT1, SMCT1), affecting gene expression through HDACs, PPARγ and Nrf2, promoting energy metabolism and changing the concentration of other metabolites (including AGEs, LPS, BHB) in the circulation to affect the body's life activities. In this paper, we focus on the possible mechanism of the primary metabolite butyrate of Roseburia intestinalis in inhibiting VC, which may become a potential therapeutic target for the treatment of VC and the ways to enhance its effect.

Keywords: Butyrate; Gut microbiome; HDACs; Roseburia intestinalis; Targeted therapy; Vascular calcification.

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Conflict of interest statement

The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.

Figures

Fig. 1
Fig. 1
Butyrate may inhibit vascular calcification. Butyrate may inhibit the transformation of VSMCs from contractile to osteogenic and vascular calcification by inhibiting macrophage inflammatory response and endothelial dysfunction. Butyrate improves the intestinal barrier by promoting mucus secretion and improving tight junctions to inhibit LPS to promote VC.
Fig. 2
Fig. 2
Some factors are conducive to increasing the abundance of R.intestinalis to increase butyrate. Diet, exercise, prebiotics, probiotics, medication and FMT may increase the abundance of R. intestinalis to increase butyrate. Butyrate inhibits a series of inflammatory reactions mediated by the NF-κB signaling pathway. Then, it inhibits vascular calcification by increasing insulin and inhibiting glucagon secretion to inhibit the content of ACEs, improving the intestinal barrier to inhibit the content of LPS, and promoting the ketogenic effect to increase the content of BHB in the blood.

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