Systemic bone loss following myocardial infarction in mice.

ABSTRACT: Myocardial infarction (MI) and osteoporotic fracture are leading causes of morbidity and mortality, and epidemiological evidence linking their incidence suggests possible crosstalk. MI can exacerbate atherosclerosis through the sympathetic nervous system (SNS) activation and β₃ adrenoreceptor-mediated release of hematopoietic stem cells, leading to monocytosis. We hypothesized that this same pathway initiates systemic bone loss following MI, since osteoclasts differentiate from monocytes. In this study, MI was created with left anterior descending artery ligation in 12-week-old male mice (n = 24) randomized to β₃ -adrenergic receptor (AR) antagonist (SR 59230A) treatment or no treatment for 10 days postoperatively. Additional mice (n = 21, treated and untreated) serve

SUBMITTER: Tjandra PM 

PROVIDER: S-EPMC8218775 | biostudies-literature | 2021 Apr

REPOSITORIES: biostudies-literature