**Figure 5.** **Silencing of lncRNA SNHG7 alleviated TGF-β1-induced fibrogenesis in cardiac fibroblasts.** (**A**, **B**) Suppression of SNHG7 attenuated the increase in collagen 1^{α}1 and collagen 3^{α}1 expression induced by TGF-β1, as measured by qRT-PCR; GAPDH mRNA served as an internal control. Data was presented as mean ± SEM; one-way ANOVA was used for the statistical analysis. n=5 independent cell cultures. (**C**) Western blotting analysis showing that knockdown of SNHG7 attenuated TGF-β1-induced fibrotic protein expression (Collagen I and α-SMA); GAPDH served as a loading control. Data was presented as mean ± SEM; one-way ANOVA was used for the statistical analysis. n=5 independent cell cultures. (**D**) MTT assay for the assessment of cell viability. Transfection of si-SNHG7 with or without AMO-34-5p in cardiac fibroblasts treated with TGF-β1 for 24h. Data was presented as mean ± SEM; one-way ANOVA was used for the statistical analysis. n=5 independent cell cultures. (**E**) EdU staining for the assessment of cell proliferation in cardiac fibroblasts inhibiting SNHG7 in the presence or absence of AMO-34-5p mimics. Scale bars represented 50 μm. (**F**) Representative images of immunofluorescence staining showing that knockdown of SNHG7 abated the TGF-β1-induced fibroblast-myofibroblast transition, which was promoted by AMO-34-5p. Scale bars represented 50 μm. ***P*<0.05.