Bone is constantly being broken down and remodeled. Osteoporosis results when bone resorption outpaces bone regeneration. Production of reactive oxygen species, a form of oxidative stress, has been predicted to promote bone loss, but a source of reactive oxygen is unknown.
In this issue of the Journal of Clinical Investigation , Katrin Schröder and colleagues at Goethe-University identify a relationship between NADPH oxidase 4 (NOX4), an enzyme that promotes reactive oxygen species formation, and bone resorption. In a mouse model of osteoporosis, genetic disruption or drug-induced loss of NOX4 protected the mice from bone loss. Additionally, the authors identify a small nuclear polymorphism in NOX4 in human patients that associated with increased bone turnover. Together, these data suggest treatments targeting NOX4 activity may benefit osteoporosis patients.
TITLE: NADPH oxidase 4 limits bone mass by promoting osteoclastogenesis
AUTHOR CONTACT: Katrin Schröder
Klinikum der Johann-Wolfgang-Goethe-Universität, Frankfurt, UNK, DEU
Phone: 004969630183660; Fax: ; E-mail: schroeder@vrc.uni-frankfurt.de
View this article at: http://www.jci.org/articles/view/67603?key=b63670ba8b7f0b31366d
Journal of Clinical Investigation