Progeroid syndrome as a model for impaired bone formation in senile osteoporosis.
Senile or age-related/dependent osteoporosis is caused by reduced bone formation, rather than increased bone resorption as in postmenopausal osteoporosis. Here we review genetically engineered mouse models with defects in osteoblastic proliferation or differentiation with focus on IGF signaling and stem cells. Model mice for human progeroid syndromes may provide useful tools for studying the pathogenesis of senile osteoporosis.
Hishiya
Akinori
A
Department of Bone and Joint Disease, Research Institute, National Center for Geriatrics and Gerontology (NCGG), 36-3 Gengo, Morioka-cho, 474-8522, Obu, Japan.
Watanabe
Ken
K
D000375:Aging / Q000502:physiology; D019588:Aging, Premature / Q000209:etiology; D000818:Animals; D002454:Cell Differentiation / Q000502:physiology; D003057:Cockayne Syndrome / Q000209:etiology / Q000503:physiopathology*; D004195:Disease Models, Animal; D005260:Female; D006801:Humans; D051379:Mice; D018345:Mice, Knockout; D010006:Osteoblasts / Q000166:cytology / Q000473:pathology*; D010012:Osteogenesis / Q000502:physiology*; D010024:Osteoporosis / Q000209:etiology / Q000503:physiopathology*; D015398:Signal Transduction; D013002:Somatomedins / Q000378:metabolism
D013002:Somatomedins