Objective      Krüppel-like factor 15 (KLF15) is a transcription factor and its expression is lost in the cardiac remodeling process associated with pathological cardiac hypertrophy prior to heart failure progression. We explored the role of KLF15 in the myocardial fibrosis process.       Methods      Cardiac fibroblasts of rats were cultured in vitro and then we developed a cell hypertrophy model. The cardiac fibroblasts were treated with KLF15 siRNA or KLF15 expression adenoviruses. The morphology of cell cli

mbing slice was observed. Collagens type Ⅰ and type Ⅲ were detected by enzyme-linked immunosorbent assay (ELISA). protein expression levels of KLF15

transforming growth factor-β (TGF-β)

connective tissue growth factor (CTGF) and myocardin-related transcription factor A (MRTF-A) were determined by Western blotting.       Results      The cardiac fibroblasts treated with KLF15 expression adenoviruses showed significant overexpression of KLF15 (P0.05) and reduced expression of collagen type Ⅰ

collagen type Ⅲ

TGF-β

CTGF and MRTF-A (

P

0.05)

and displayed relieved hypertrophy and fibrosis. However

the cardiac fibroblasts treated with KLF15 siRNA had contrary results (

P

0.05).       Conclusion      KLF15 inhibits cardiac interstitial fibrosis and cardiac fibroblast phenotypic transformation by feedback controlling of TGF-β and expression inhibition of CTGF and MRTF-A. The cardiac function is markedly ameliorated.