Skip to main content
. Author manuscript; available in PMC: 2024 Nov 14.
Published in final edited form as: Circulation. 2023 Sep 18;148(20):1582–1592. doi: 10.1161/CIRCULATIONAHA.123.066002

Figure 6. Inhibition of DDR signaling inhibits pressure overload–induced cardiomyocyte hypertrophy in cs-Snrk−/−.

Figure 6.

A-D, EF (A), FS (B), PWTd (C), and LVDs (D) in WT and cs-Snrk−/− mice 4-weeks after sham operation or TAC with or without KU-60019 (n=6, two-way ANOVA with Holm-Sidak’s multiple comparisons test). *P<0.05, **P<0.01, ***P<0.001, ****P<0.0001. E, Schematic model for the SNRK-DSTN interaction in relation to SNRK KO hypertrophy. SNRK regulates nuclear morphology and DDR through DSTN mediated actin depolymerization, and that deletion of Snrk leads to cardiac hypertrophy through perturbation of G/F actin ratio.