RESUMEN
Aim To explore the regulatory effect of lncRNA-ZFASl on myocardial fibrosis. Methods The mouse model of myocardial fibrosis was established by ligating the left anterior descending coronary artery of heart; the lncRNA-ZFASl cardiac-specific transgenic mice were constructed by CRISPR/Cas9 technology. Masson staining was used to detect the fibrosis of heart tissues ; angiotensin E ( Ang H ) was added to cardiac fibroblasts to establish an in vitro myocardial fibrosis model, and siRNA was transfected to knock down lncRNA-ZFASl ; MTT method was used to detect the proliferation of cardiac fibroblasts; real-time quantitative PCR ( qRT-PCR ) was used to detect the expression of lncRNA-ZFASl, transforming growth factor ßl (TGFßl), type I collagen (Collai) and type M col¬lagen (Col3al). Western blot was used to detect a-SMA expression. Results In cardiac tissues of myo¬cardial fibrosis model mice, the expression of lncRNA-ZFASl significantly increased. Knocking down of lncRNA-ZFASl significantly reduced the expression of CoBal and TGFßl in Ang II treated cardiac fibroblasts. Collagen deposition appeared in cardiac tissues of lncRNA-ZFASl transgenic mice, and the expression of a-SMA, Collai and CoBal markedly increased. Conclusions The high expression of lncRNA-ZFASl in heart tissues could induce myocardial fibrosis, and knocking down lncRNA-ZFASl could alleviate myocardial fibrosis.