Fig. 10: Changes induced by pressure overload in MCM-TRPV2-cKO mice.

a Histological analysis 2, 8, and 16 weeks after pressure overload induction. Scale bar, 5 mm. b Changes in cross-sectional area of cardiomyocytes (n = 144–504 cells from 3 mice per group). Centre line = median; + = mean; box limits = upper and lower quartiles, whiskers = minimum and maximum. c Changes in heart-to-body weight (HW/BW) ratio (N = 5–6 mice per group). d, e Echocardiographic assessment of left ventricular end dimension at systole and fractional shortening (N = 10 mice per group). *P < 0.05 in multiple comparisons based on Tukey–Kramer test. f Representative tracing of two-dimensional transthoracic M-mode echocardiography. g Echocardiographic assessment of interventricular septal thickness at end-diastole. *P < 0.05 in multiple comparisons based on Tukey–Kramer test. # P < 0.05 vs. pre-TAC Floxed-TRPV2 based on Student’s t-test. h Fibrosis percentage (N = 3 hearts per group). i Representative immunoblots of hearts treated with vehicle or TAC after 16 weeks. (N = 3 mice) *P < 0.05 vs. multiple comparisons based on Tukey–Kramer test. j Estimated TRPV2 signal pathway affecting maturation and pathological remodelling. Data are shown as mean ± standard error of the mean (SEM).