| First Author | Zou SF | Year | 2020 |
| Journal | Mol Med Rep | Volume | 21 |
| Issue | 3 | Pages | 1336-1345 |
| PubMed ID | 31922214 | Mgi Jnum | J:343820 |
| Mgi Id | MGI:6884477 | Doi | 10.3892/mmr.2020.10913 |
| Citation | Zou SF, et al. (2020) KLF15 is a protective regulatory factor of heart failure induced by pressure overload. Mol Med Rep 21(3):1336-1345 |
| abstractText | The aim of the present study was to investigate the protective effect of Kruppellike factor 15 (KLF15) overexpression on heart failure (HF) induced by left ventricular (LV) pressure overload in mice. Wildtype (WT) mice and cardiacspecific KLF15overexpressed transgenic (TG) mice were selected as research subjects, and an LV pressure overload model was constructed by ascending aortic constriction surgery. Changes in cardiac morphology and function, and ultrastructure and molecular expression were observed via Mmode echocardiography, histological and immunohistochemical staining, ELISA and western blotting at 2 and 6 weeks of LV overload. WT and TG mice subjected to 2 weeks of overload displayed adaptive LV hypertrophy characterized by ventricular thickness, cardiomyocyte size, ejection fraction and fractional shortening of heartlung weight ratio and KLF15, and increases in vascular endothelial growth factor (VEGF) expression without other pathological changes. WT mice subjected to 6 weeks of overload displayed enlargement of the LV chamber, severe interstitial remodeling, and HW/LW, cardiac capillary and heart function decline, accompanied by downregulated expression of KLF15 and VEGF, and upregulated expression of connective tissue growth factor, phosphorylated p38 (pp38) and phosphorylated Smad3 (pSmad3). In contrast, TG mice exhibited improved resistance to 6 weeks of overload and a slighter molecular expression response compared with WT mice. KLF15 was revealed to be a critical factor regulating the expression of CTGF, VEGF, pp38 and pSmad3, and could alleviate the progression from adaptive LV hypertrophy to decompensatory cardiac insufficiency. |
