Fig. 3From: Gut microbiota from coronary artery disease patients contributes to vascular dysfunction in mice by regulating bile acid metabolism and immune activationMicrobiota from CAD patients cause imbalanced bile acids profiles and regulate genes involved in BA synthesis. a Relative amounts of bile acids categories in the serum and faeces of Con and CAD mice. b UPLC-MS/MS analyses of bile acids in the faeces significantly changed. c Gene expression of Fgfr 4 in the liver. d The graphs represent gene expression of enzymes involved in bile acids biosynthesis in the liver. e The proportion of CA/CDCA ratio in the faeces. f Concentrations of bile acids significantly changed in the serum. g Secondary bile acids abundance in CAD patients (N = 6) and healthy volunteer donors (N = 5). Mean values ± SEM are plotted; *P < 0.05, **P < 0.01, ***P < 0.001, ****P < 0.0001, Mann–Whitney U test. Con colonization with microbiota from healthy donors, n = 9-11; CAD, colonization with microbiota from coronary artery disease patients, n = 10-12. BAs, bile acids; CA, cholic acid; CDCA, chenodeoxycholic acid; MCA, muricholic acid; DCA, deoxycholic acid; HDCA, hyodeoxycholic acid; LCA, lithocholic acid; UDCA, ursodeoxycholic acid; T, taurine-conjugatedBack to article page