Osteocrin (OSTN) is a secretory peptide mainly derived from the skeletal muscles and bones. The present study aims to explore the role of OSTN in cardiac hypertrophy and its underlying mechanism. Experiments were carried out in mice receiving angiotensin (Ang) II to induce cardiac hypertrophy, and in neonatal rat cardiomyocytes (NRCMs) or human cardiac AC16 cells with Ang II-induced cardiomyocytes hypertrophy. The expression of OSTN was lower in Ang II-treated mouse heart of mice, NRCMs and AC16 cells. OSTN overexpression attenuated the hypertrophy and fibrosis of heart in mice induced by Ang II. Overexpression of OSTN inhibited hypertrophy of NRCMs and AC16 cells induced by Ang II. Increased oxidative stress was observed in the heart of mice, NRCMs and AC16 cells treated with Ang II. Overexpression of NADPH oxidase 1 (Nox1) reversed the attenuating effects of OSTN on the Ang II-induced hypertrophic cardiomyocytes. Treatment with NADPH oxidase inhibitor apocynin (APO) suppressed the hypertrophy of NRCMs and AC16 cells induced by Ang II. The above findings suggested OSTN upregulation could attenuate cardiac hypertrophy and fibrosis. The upregulation of OSTN could alleviate hypertrophy of cardiomyocytes via suppressing oxidative stress.
Keywords: Cardiomyocyte; Hypertrophy; Osteocrin; Oxidative stress.
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