骨吸收
吸收
内分泌学
内科学
脆性骨折
医学
脆弱性
骨重建
骨质疏松症
化学
骨矿物
物理化学
作者
Elizabeth M. Hennen,Sasidhar Uppuganti,Néstor de la Visitación,Wei Chen,Jaya Krishnan,Lawrence A. Vecchi,David M. Patrick,Mateusz Siedliński,Matteo Lemoli,Rachel Delgado,Mark deCaestecker,Wenhan Chang,Tomasz J. Guzik,Rachelle W. Johnson,David G. Harrison,Jeffry S. Nyman
摘要
Inflammatory diseases contribute to secondary osteoporosis. Hypertension is a highly prevalent inflammatory condition that is clinically associated with reduced bone mineral density and increased risk for fragility fracture. In this study, we showed that a significant loss in bone mass and strength occurs in two pre-clinical models of hypertension. This accompanied increases in immune cell populations, including monocytes, macrophages, and IL-17A-producing T cell subtypes in the bone marrow of hypertensive mice. Neutralizing IL-17A in angiotensin (ang) II-infused mice blunted hypertension-induced loss of bone mass and strength due to decreased osteoclastogenesis. Likewise, the inhibition of the CSF-1 receptor blunted loss of bone mass and prevented loss of bone strength in hypertensive mice. In an analysis of UK Biobank data, circulating bone remodeling markers exhibited striking associations with blood pressure and bone mineral density in > 27,000 humans. These findings illustrate a potential mechanism by which hypertension activates immune cells in the bone marrow, encouraging osteoclastogenesis and eventual loss in bone mass and strength.
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