Fig. 6: AAV9:mMybpc3 improved diastolic dysfunction in Mybpc3-/- mice. | Nature Communications

Fig. 6: AAV9:mMybpc3 improved diastolic dysfunction in Mybpc3-/- mice.

From: AAV9-mediated MYBPC3 gene therapy with optimized expression cassette enhances cardiac function and survival in MYBPC3 cardiomyopathy models

Fig. 6

Homozygous mice were dosed retro-orbitally IV with vehicle or 3E13 vg/kg of AAV9:mMybpc3 at two weeks of age and assessed for diastolic dysfunction 12 weeks post-injection. a Representative tissue (top) and pulsed-wave transmitral (bottom) Doppler tracings. Mitral annular e’ velocity, maximal mitral E-wave velocity (E), and maximal mitral A-wave velocity (A) shown. b Quantitation of mitral E-wave velocity (MV E), c mitral annular e’ velocity, and d isovolumic relaxation time (IVRT) demonstrated dysfunction in Mybpc3-/- mice that was ameliorated by treatment, n = 9 (5 M/4 F)/group. P-value per one-way ANOVA with Tukey’s multiple comparisons test. Data are shown as means ± SEM. Source data are provided as a Source Data file.

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