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Deferoxamine synergizes with transforming growth factor-ß signaling in chondrogenesis.
Huang, Zheng; He, Guangxu; Huang, Yanke.
Afiliação
  • Huang Z; Department of Spinal Surgery, Shenzhen Nanshan Hospital of Guangdong Medical College, Shenzhen, Guangdong, China.
  • He G; Department of Orthopedics, Second Xiangya Hospital, Central South University, Changsha, Hunan, China.
  • Huang Y; Clinic of Psychology, Shenzhen Nanshan Maternity and Child Healthcare Hospital, Shenzhen, Guangdong, China.
Genet Mol Biol ; 40(3): 698-702, 2017.
Article em En | MEDLINE | ID: mdl-28810001
Osteoarthritis, also known as degenerative arthritis or degenerative joint disease, is an epidemic disease that affects millions of people worldwide. Despite extensive recent work on the cellular biology of osteoarthritis, the precise mechanisms involved are still poorly understood and there is no effective treatment for this disease. The role of transforming growth factor-beta (TGF-ß) in promoting chondrogenesis and inducing the expression of cartilage-specific extracellular matrix molecules to form cartilage is well-established. Historically, TGF-ß has been considered to prevent osteoarthritis, but recent work suggests that TGF-ß overexpression accelerates the progression of osteoarthritis in vivo. Clinically, it is therefore important to limit TGF-ß expression while still providing effective treatment of osteoarthritis. One possible approach to achieve this effect would be to use a combination of TGF-ß with other small molecular chemical compounds. Hypoxia promotes chondrogenesis and the usefulness of deferoxamine, a chelating agent that mimics hypoxia, in stimulating chondrogenesis has been investigated in clinical trials. In this study, we investigated the role of deferoxamine in TGF-ß-induced chondrogenesis in pre-chondrogenic cells and examined whether deferoxamine synergizes with the TGF-ß signaling pathway to promote chondrocyte differentiation.

Texto completo: 1 Coleções: 01-internacional Base de dados: MEDLINE Idioma: En Revista: Genet Mol Biol Ano de publicação: 2017 Tipo de documento: Article País de afiliação: China País de publicação: Brasil

Texto completo: 1 Coleções: 01-internacional Base de dados: MEDLINE Idioma: En Revista: Genet Mol Biol Ano de publicação: 2017 Tipo de documento: Article País de afiliação: China País de publicação: Brasil