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Fig. 4 | Journal of Translational Medicine

Fig. 4

From: Gut microbiota from coronary artery disease patients contributes to vascular dysfunction in mice by regulating bile acid metabolism and immune activation

Fig. 4

Gut microbiota variation and association with BAs metabolism after faecal microbiota transplantation. a Barterial communities from human donors and recipient mouse were clustered using PCoA analysis of the Bray–Curtis distance matrix. b Phylum-level changes of human donors and recipient mouse, showing average percentages of each phylum as a proportion of the whole community. c Relative abundance of KO genes involved in secondary bile acids metabolism that showed significant difference between Con and CAD groups are shown in the heat map. Significant changes (elevation and depletion) are denoted as follows: *P < 0.05; #P < 0.01. Representative KO genes are shown in pathway modules modified from KEGG pathway maps ‘Secondary bile acid metabolism’. d Spearman correlations between bacterial relative gene abundance and faecal bile acid levels. e Abundance of species between Con versus CAD comparison contributing to secondary BAs transformation. Boxes represent the inter-quartile ranges, and lines inside the boxes denote medians. *P < 0.05, **P < 0.01, Wilcoxon rank sum test. Con mice, n = 10-11; CAD mice, n = 11-12. BSH, bile salt hydrolase; HDSH, hydroxysteroid dehydrogenases; BAs, bile acids; CA, cholic acid; CDCA, chenodeoxycholic acid; DCA, deoxycholic acid; LCA, lithocholic acid; Con, colonization with microbiota from healthy donors; CAD, colonization with microbiota from coronary artery disease patients

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