Fasudil Ameliorates Osteoporosis Following Myocardial Infarction by Regulating Cardiac Calcitonin Secretion.

Abstract

We hypothesis that Rho kinase inhibitor fasudil ameliorates osteoporosis following myocardial infarction (MI) by regulating cardiac calcitonin secretion. A mice model of MI and cultured neonatal cardiomyocytes exposed to hypoxia and serum deprivation (H/SD), and fibroblasts exposed to TGF-β were used, respectively. Cardiac function in vivo was assessed with echocardiography. Osteoporosis in vivo was assessed with X-ray and micro-CT. In vivo and in vitro studies used histological and immunohistochemical techniques, along with western blots. In mice post-MI, fasudil ameliorates the microstructure and bone metabolism of the lumbar, improved cardiac function, and attenuated myocardial fibrosis. In vitro, fasudil or αCGRP could effectively inhibit the proliferation of primary fibroblasts treated with TGF-β. Moreover, fasudil ameliorates the cardiac calcitonin secretion induced by MI in vivo or by H/SD in vitro. Our findings suggest that fasudil improved MI-induced osteoporosis by promoting cardiac secreting calcitonin.

• Authors: Chengyu Xiang, Yeqian Zhu, Maohua Xu, Dingguo Zhang
• Journal: Journal of cardiovascular translational research (J Cardiovasc Transl Res) Vol. 15 Issue 6 Pg. 1352-1365 (12 2022) ISSN: 1937-5395 [Electronic] United States
• PMID: 35551627 (Publication Type: Journal Article)
• Copyright: © 2022. The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature.

Chemical References

• Calcitonin
• fasudil
• Transforming Growth Factor beta

Topics

• Animals
• Mice
• Calcitonin (metabolism)
• Fibrosis
• Myocardial Infarction (complications, drug therapy, metabolism)
• Myocardium (pathology)
• Myocytes, Cardiac (metabolism)
• Osteoporosis (drug therapy, etiology, metabolism)
• Transforming Growth Factor beta (pharmacology)