Effect of rapamycin on bone mass and strength in the α2(I)‐G610C mouse model of osteogenesis imperfecta

Osteogenesis imperfecta (OI) is commonly caused by heterozygous type I collagen structural mutations that disturb triple helix folding and integrity. This mutant‐containing misfolded collagen accumulates in the endoplasmic reticulum (ER) and induces a form of ER stress associated with negative effec...

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Veröffentlicht in:	Journal of cellular and molecular medicine 2019-03, Vol.23 (3), p.1735-1745
Hauptverfasser:	Bateman, John F., Sampurno, Lisa, Maurizi, Antonio, Lamandé, Shireen R., Sims, Natalie A., Cheng, Tegan L., Schindeler, Aaron, Little, David G.
Format:	Artikel
Sprache:	eng
Schlagworte:	Animals Apoptosis Autophagy autophagy stimulation biomechanics Bone Density - drug effects Bone growth Bone mass Bones Collagen Collagen (type I) Collagen Type I - physiology Disease Models, Animal diseases and disorders of bone Endoplasmic reticulum Female Immunosuppressive Agents - pharmacology Male Mechanical properties Mice Mice, Inbred C57BL Mice, Mutant Strains micro‐computed tomography Mutation Original Osteoblastogenesis Osteoblasts - cytology Osteoblasts - drug effects Osteogenesis Osteogenesis imperfecta Osteogenesis Imperfecta - drug therapy Osteogenesis Imperfecta - metabolism Osteogenesis Imperfecta - pathology Phagocytosis Rapamycin rapamycin treatment Sirolimus - pharmacology
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