Usage Information

Hypertension promotes bone loss and fragility by favoring bone resorption in mouse models
Elizabeth M. Hennen, Sasidhar Uppuganti, Néstor de la Visitación, Wei Chen, Jaya Krishnan, Lawrence A. Vecchi III, David M. Patrick, Mateusz Siedlinski, Matteo Lemoli, Rachel Delgado, Mark P. de Caestecker, Wenhan Chang, Tomasz J. Guzik, Rachelle W. Johnson, David G. Harrison, Jeffry S. Nyman
Elizabeth M. Hennen, Sasidhar Uppuganti, Néstor de la Visitación, Wei Chen, Jaya Krishnan, Lawrence A. Vecchi III, David M. Patrick, Mateusz Siedlinski, Matteo Lemoli, Rachel Delgado, Mark P. de Caestecker, Wenhan Chang, Tomasz J. Guzik, Rachelle W. Johnson, David G. Harrison, Jeffry S. Nyman
View: Text | PDF
Research Article Bone biology Immunology Inflammation

Hypertension promotes bone loss and fragility by favoring bone resorption in mouse models

Abstract

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 of fragility fracture. In this study, we showed that a significant loss in bone mass and strength occurs in two preclinical 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 II–infused mice blunted hypertension-induced loss of bone mass and strength as a result of decreased osteoclastogenesis. Likewise, the inhibition of the CSF1 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 more than 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.

Authors

Elizabeth M. Hennen, Sasidhar Uppuganti, Néstor de la Visitación, Wei Chen, Jaya Krishnan, Lawrence A. Vecchi III, David M. Patrick, Mateusz Siedlinski, Matteo Lemoli, Rachel Delgado, Mark P. de Caestecker, Wenhan Chang, Tomasz J. Guzik, Rachelle W. Johnson, David G. Harrison, Jeffry S. Nyman

×

Usage data is cumulative from August 2025 through May 2026.

Usage JCI PMC
Text version 4,499 293
PDF 1,420 77
Figure 1,271 2
Supplemental data 424 21
Citation downloads 207 0
Totals 7,821 393
Total Views 8,214

Usage information is collected from two different sources: this site (JCI) and Pubmed Central (PMC). JCI information (compiled daily) shows human readership based on methods we employ to screen out robotic usage. PMC information (aggregated monthly) is also similarly screened of robotic usage.

Various methods are used to distinguish robotic usage. For example, Google automatically scans articles to add to its search index and identifies itself as robotic; other services might not clearly identify themselves as robotic, or they are new or unknown as robotic. Because this activity can be misinterpreted as human readership, data may be re-processed periodically to reflect an improved understanding of robotic activity. Because of these factors, readers should consider usage information illustrative but subject to change.

Advertisement