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Osteoblast autophagy in glucocorticoid-induced osteoporosis.
Wang, Lufei; Heckmann, Bradlee L; Yang, Xianrui; Long, Hu.
  • Wang L; Oral and Craniofacial Biomedicine Program, School of Dentistry, University of North Carolina at Chapel Hill, Chapel Hill, North Carolina.
  • Heckmann BL; Department of Immunology, St. Jude Children's Research Hospital, Memphis, Tennessee.
  • Yang X; Department of Orthodontics, State Key Laboratory of Oral Diseases, National Clinical Research Center for Oral Diseases, West China Hospital of Stomatology, Sichuan University, Chengdu, China.
  • Long H; Department of Developmental Biology, Harvard School of Dental Medicine, Boston, Massachusetts.
J Cell Physiol ; 234(4): 3207-3215, 2019 04.
Article en En | MEDLINE | ID: mdl-30417506
ABSTRACT
Administration of glucocorticoids is an effective strategy for treating many inflammatory and autoimmune diseases. However, glucocorticoid treatment can have adverse effects on bone, leading to glucocorticoid-induced osteoporosis (GIO), the most common form of secondary osteoporosis. Although the pathogenesis of GIO has been studied for decades, over the past ten years the autophagy machinery has been implicated as a novel mechanism. Autophagy in osteoblasts, osteocytes, and osteoclasts plays a critical role in the maintenance of bone homeostasis. Herein, we specifically discuss how osteoblast autophagy responds to glucocorticoids and its role in the development of GIO.
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Texto completo: 1 Banco de datos: MEDLINE Asunto principal: Osteoblastos / Osteoporosis / Autofagia / Glucocorticoides Límite: Animals / Humans Idioma: En Año: 2019 Tipo del documento: Article

Texto completo: 1 Banco de datos: MEDLINE Asunto principal: Osteoblastos / Osteoporosis / Autofagia / Glucocorticoides Límite: Animals / Humans Idioma: En Año: 2019 Tipo del documento: Article