Increased expression of secreted frizzled related protein 3 (SFRP3) is associated with adverse outcomes of heart failure. The purpose of this study was to investigate the effect of SFRP3 on cardiac remodeling and its mechanism. Cardiac remodeling was induced by angiotensin II (Ang II) infusion in the mice, and in the neonatal rat cardiomyocytes (NRCM) treated with Ang II. The expression decreased in the heart of mice, and NRCM and HL-1 cells with Ang II treatment. Ang II-induced hypertrophy and fibrosis of heart in mice were attenuated by upregulation of SFRP3, and were further deteriorated by downregulation of SFRP3. Ang II-induced hypertrophy of NRCM and HL-1 cells were improved by SFRP3 overexpression, and were further deteriorated by SFRP3 knockdown. The oxidative stress increased in the heart of Ang II-treated mice, and this enhancement was inhibited by overexpressing of SFPR3, and was worsened by downregulation of SFPR3. These outcomes suggested that upregulation of SFPR3 could improve cardiac remodeling via inhibition of oxidative stress.
Keywords: Cardiac remodeling; Cardiomyocytes; Frizzled related protein 3; Oxidative stress.
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