Fig. 9.

Overexpressing Mfn1 reversed the aggravation of myocardial infarction and microvascular dysfunction induced by silencing Malat1 in MI hearts. One-week overall survival curve (A). The M-mode of echocardiography images and the data on left ventricular end-diastolic diameter (LVEDD), ejection fraction (EF) and fractional shortening (FS) for each group (B, C). Heart weight to body weight ratio (HW/BW) of each group (D). Analysis of serum brain natriuretic peptide (BNP) levels (E). HE staining, Masson staining and quantification of cardiac fibrosis (F, G). Analysis of serum cardiac troponin T (cTnT) concentration and lactate dehydrogenase (LDH) activity (H, I). Microvascular perfusion of the border zone was indicated by the ratio of lectin-perfused vessels (green) to CD31-positive ECs (red) (J). Immunofluorescence staining for eNOS (K). Nitric oxide (NO) content in the border zone of each group (L). Immunofluorescence staining for VEGFR2 (M). eNOS expression and phosphorylation at Ser¹¹⁷⁷ in the border zone were analysed by Western blotting (N). VEGFR2 expression and phosphorylation at Tyr¹¹⁷⁵ in the border zone were analysed by Western blotting (O).*p < 0.05 compared with the sham + Scr-shRNA + vector group, #p < 0.05 compared with the MI + Scr-shRNA + vector group, & p < 0.05 compared with the MI + Malat1-shRNA + vector group. n = 6 in each group.