Skip to main content
. Author manuscript; available in PMC: 2020 Aug 13.
Published in final edited form as: Circulation. 2019 Jun 10;140(7):566–579. doi: 10.1161/CIRCULATIONAHA.118.038924

Figure 1. Cardiac-specific deficiency of XBP1s leads to cardiomyopathy in mice.

Figure 1.

A. XBP1s expression was reduced in the hearts from human patients with dilated cardiomyopathy (DCM). N = 6 for normal controls; 7 for DCM. XBP1s expression was decreased in failing mouse hearts. Cardiac dilation and heart failure were triggered by thoracic aortic constriction (TAC). N = 5 for each group. Student’s t test was conducted.

B. Cardiac-specific knockout of XBP1s caused early mortality. XBP1s deletion was achieved by crossing XBP1F/F with the αMHC-Cre mouse models. All conditional knockout (cKO) mice died before 350 days old, while the controls did not show mortality. N = 14 for F/F; 6 for αMHC-Cre; 14 for cKO. The log rank test was conducted. P<0.001 between F/F and cKO, and Cre and cKO, respectively.

C. XBP1s cKO mice showed gradual deterioration of cardiac function. Fractional shortening (%) was determined by echocardiography with conscious animals. N = 5 per group.

D. XBP1s deficient mice displayed an increase in left ventricular inner diameter (LVID) at diastole. N = 5 for each group.

E. XBP1s cKO showed elevated left ventricular diameter at systole. N = 5 for each group. Two-way ANOVA was conducted with the selection of repeated measures, followed by Bonferroni’s multiple comparisons test. *, P<0.05; **, P<0.01; ***, P<0.001.