FXR agonists improve obesity-induced fibrinolysis impairment and high DVT burden. (A-H) MPHs were treated with palmitic acid for 6 hours and subsequently coincubated with FXR agonists (CDCA and tropifexor) for the next 6 hours: (A) Serpine1 mRNA (N = 5); (B) PAI-1 concentration in medium (N = 5); (C-D) PAI-1 protein (N = 5). (E-R) Obese mice treated with tropifexor were randomly selected for DVT modeling or other assays (N = 4): (E) liver Nr0b2 mRNA (N = 4); (F) liver Abcb11 mRNA (N = 4); (G) liver Serpine1 mRNA (N = 4); (H) plasma PAI-1 levels (N = 4); (I-J) tail bleeding time (N = 9); (K-M) thrombus weight and length (N = 5); (N-R) representative curves for plasma fibrin formation and lysis tests and parameters of the curves for fibrinolysis (N = 4). The data are represented as the mean ± SEM, n.s. P > .05; ∗P < .05; ∗∗P < .01 vs PA600 or HFD group. BSA, bovine serum albumin; BT, bleeding time; GAPDH, glyceraldehyde-3-phosphate dehydrogenase; LJN452, tropifexor; n.s., no significance; PA, palmitic acid.