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. Author manuscript; available in PMC: 2015 Mar 19.
Published in final edited form as: Sci Transl Med. 2013 Oct 16;5(207):207ra141. doi: 10.1126/scitranslmed.3006479

Fig. 7. TNNI3K inhibition reduces chronic LV dysfunction and limits progressive remodeling after MI/R.

Fig. 7

C57BL/6 mice were subjected to 40 min of LV ischemia. GSK854 (2.75 mg/kg intraperitoneally) was administered at reperfusion and at 6 hours after reperfusion. Animals were then placed on GSK854 (100 mg/kg; in chow) for 6 weeks. (A) Representative low-magnification images from n = 3 (sham groups) or n = 10 (MI/R groups) hearts stained with Masson’s trichrome stain. Scale bar, 1 mm. (B) Ejection fraction (%EF) at 2 and 4 weeks after MI/R, measured by two-dimensionally directed M-mode echocardiography. (C and D) LV end-systolic dimension and LV end-diastolic dimension as measured by M-mode echocardiography 4 weeks after MI/R. (E) Plasma pro-ANP levels assessed by enzyme-linked immunosorbent assay in the various groups at 6 weeks after MI/R. (F) Heart weight/body weight ratios at 6 weeks after MI/R. (G) Cardiomyocyte cross-sectional area (CSA) in the above groups as measured from the LV of hematoxylin and eosin–stained sections. (H) Quantification of fibrosis for the hearts shown in (A). All data are shown as means ± SEM. *P < 0.05, **P < 0.01, ***P < 0.001 as determined by one-way ANOVA followed by Tukey’s post hoc test. NS, not significant.