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Nell-1 in bone tissue engineering / 中国组织工程研究
Chinese Journal of Tissue Engineering Research ; (53): 3217-3225, 2020.
Artigo em Chinês | WPRIM | ID: wpr-847480
ABSTRACT

BACKGROUND:

Nel-like type 1 molecule (Nell-1) is a secreted glycoprotein that has been proven both in vitro and in vivo to be a potent osteoinductive factor that effectively promotes bone growth. Furthermore, it has been shown to repress adipogenic differentiation and inflammation.

OBJECTIVE:

To review the current research progress of Nell-1 in bone tissue engineering.

METHODS:

PubMed database was searched for relevant articles published from January 1996 to June 2019. Search words were “Nell-1; bone regeneration and repair; regulatory factor; signal path; bone morphogenetic protein; osteoporosis; marrow derived mesenchymal stem cells.” After removal of repetitive studies and inconsistent literature, 61 articles were finally analyzed. RESULTS AND

CONCLUSION:

Nell-1 has been proved to be a factor that can effectively promote bone tissue growth. Local application of Nell-1 has a good effect on the growth of long bone, spine and cartilage as well as cranial suture closure. Nell-1 is a new growth factor that has relatively simple bioeffects, so it has better biosafety and higher accuracy relative to the other bone growth factors. Nell-1 can synergize with other osteogenic factors such as bone morphogenetic proteins 2, 9. Nell-1 inhibits inflammatory reaction and lipogenesis induced by bone morphogenetic protein 2 and promotes osteogenesis. This provides a theoretical basis for the combination of Nell-1 and bone morphogenetic protein 2 to improve the clinical safety and efficacy in bone regeneration.

Texto completo: DisponíveL Índice: WPRIM (Pacífico Ocidental) Idioma: Chinês Revista: Chinese Journal of Tissue Engineering Research Ano de publicação: 2020 Tipo de documento: Artigo

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Texto completo: DisponíveL Índice: WPRIM (Pacífico Ocidental) Idioma: Chinês Revista: Chinese Journal of Tissue Engineering Research Ano de publicação: 2020 Tipo de documento: Artigo