{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,5,17]],"date-time":"2026-05-17T04:22:19Z","timestamp":1778991739113,"version":"3.51.4"},"reference-count":36,"publisher":"Wiley","issue":"4","license":[{"start":{"date-parts":[[2020,10,6]],"date-time":"2020-10-06T00:00:00Z","timestamp":1601942400000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"funder":[{"DOI":"10.13039\/100000069","name":"National Institute of Arthritis and Musculoskeletal and Skin Diseases","doi-asserted-by":"publisher","award":["AR071459"],"award-info":[{"award-number":["AR071459"]}],"id":[{"id":"10.13039\/100000069","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Journal Orthopaedic Research"],"published-print":{"date-parts":[[2021,4]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:p>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 \u03b2<jats:sub>3<\/jats:sub> adrenoreceptor\u2010mediated release of hematopoietic stem cells, leading to monocytosis. We hypothesized that this same pathway initiates systemic bone loss following MI,\u00a0since osteoclasts differentiate from monocytes. In this study, MI was created with left anterior descending\u00a0artery ligation in 12\u2010week\u2010old male mice (<jats:italic>n<\/jats:italic>\u2009=\u200924) randomized to \u03b2<jats:sub>3<\/jats:sub>\u2010adrenergic receptor (AR) antagonist (SR 59230A) treatment or no treatment for 10 days postoperatively. Additional mice (<jats:italic>n<\/jats:italic>\u2009=\u200921, treated and untreated) served as unoperated controls. Bone mineral density (BMD), bone mineral content (BMC), and body composition were quantified at baseline and 10 days post\u2010MI using dual\u2010energy x\u2010ray absorptiometry; circulating monocyte levels were quantified and the L5 vertebral body and femur were analyzed with microcomputed tomography 10 days post\u2010MI. We found that MI led to circulating monocyte levels increases, BMD and BMC decreases at the femur and lumbar spine in MI mice (\u22126.9% femur BMD, \u22123.5% lumbar BMD), and trabecular bone volume decreases in MI mice compared with control mice. \u03b2<jats:sub>3<\/jats:sub>\u2010AR antagonist treatment appeared to diminish the bone loss response (\u22125.3% femur BMD, \u22121.2% lumbar BMD), though these results were somewhat inconsistent. Clinical significance:\u00a0These results suggest that MI leads to systemic bone loss, but that the SNS may not be a primary modulator of this response; bone loss and increased fracture risk may be important clinical comorbidities following MI or other ischemic injuries.<\/jats:p>","DOI":"10.1002\/jor.24867","type":"journal-article","created":{"date-parts":[[2020,9,23]],"date-time":"2020-09-23T16:27:47Z","timestamp":1600878467000},"page":"739-749","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":7,"title":["Systemic bone loss following myocardial infarction in mice"],"prefix":"10.1002","volume":"39","author":[{"ORCID":"https:\/\/orcid.org\/0000-0001-8771-3422","authenticated-orcid":false,"given":"Priscilla M.","family":"Tjandra","sequence":"first","affiliation":[{"name":"Biomedical Engineering Graduate Group University of California Davis  Davis California 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