Research Paper Volume 14, Issue 14 pp 5925—5945

miR-21 upregulation exacerbates pressure overload-induced cardiac hypertrophy in aged hearts


Figure 1. Angiotensin II (Ang II)-induced cardiac hypertrophy and fibrosis, especially in aged mice. (A) Echocardiography measurements are shown in young and aged mice with or without Ang II. Systolic and diastolic blood pressures recorded. Echocardiographic measurements of intraventricular septal thickness at diastole (IVSd) and ejection fraction and fractional shortening. (B) Quantitative analysis of heart weight/tibia length. (C) Representative sections and amplified images of the highlighted area of hearts stained with Masson's trichrome for fibrosis detection (blue); scale bars, 30 μm (left panel). Quantification of cardiac fibrosis in the indicated groups of rats (right panel). Expression of (D) circulating and (E) heart tissue expression of miR-21 in mice. Data are expressed using mean ± standard deviation (S.D.). *P < 0.05, **P < 0.01, ***P < 0.001 for difference from each group (N = 6–12).