Will reducing adopogenesis in bone increase bone mass?: PPARgamma2 as a key target in the treatment of age-related bone loss.
There are several mechanisms that explain the pathophysiology of senile osteoporosis. One of them is the increasing levels of adipogenesis in bone marrow that are seen during the aging process. It is known that mesenchymal stem cells expressing a ligand-activated transcription factor known as peroxisome proliferator-activated receptor gamma(2) (PPARgamma(2)) are committed to differentiate into adipocytes. The regulation of PPARgamma(2) activation may play a role in the control of adipogenic differentiation of mesenchymal stem cells and thus contribute to their differentiation into osteoblasts in order to form new bone. In this review we describe the characteristics of the orphan receptor family of PPARs, with emphasis on PPARgamma(2), its structural and functional characteristics and its potential as a therapeutic target for the treatment of senile osteoporosis.
Duque
Gustavo
G
Division of Geriatric Medicine-McGill University, Jewish General Hospital, 3599 Cote Sainte Catherine, Montreal, Quebec, Canada. gduque@pobox.mcgill.ca
D017667:Adipocytes / Q000378:metabolism / Q000502:physiology*; D000375:Aging / Q000473:pathology; D001854:Bone Marrow Cells / Q000502:physiology; D001842:Bone and Bones / Q000473:pathology*; D002454:Cell Differentiation / Q000502:physiology; D006801:Humans; D010024:Osteoporosis / Q000378:metabolism / Q000473:pathology*; D018160:Receptors, Cytoplasmic and Nuclear / Q000037:antagonists & inhibitors* / Q000378:metabolism* / Q000502:physiology; D014157:Transcription Factors / Q000037:antagonists & inhibitors* / Q000378:metabolism* / Q000502:physiology
D018160:Receptors, Cytoplasmic and Nuclear; D014157:Transcription Factors