Vascular endothelial growth factor and hypoxia-inducible factor suppress chondrocyte apoptosis

doi:10.3969/j.issn.2095-4344.2015.29.022

Abstract

Abstract:

BACKGROUND: Osteoarthritis is a joint disease that primarily affects the cartilage. With the changes of the extracellular matrix, chondrocytes appear to have apoptosis. Vascular endothelial growth factor plays an important role in promoting endothelial cell division and proliferation and inducing angiogenesis. Hypoxia-inducible factor is a cellular transcription factor and produces different reactions due to the oxygen content. Vascular endothelial growth factor and hypoxia-inducible factor are focused on inhibiting chondrocyte apoptosis.
OBJECTIVE: To elaborate the effects of vascular endothelial growth factor and hypoxia-inducible factors on chondrocyte apoptosis.
METHODS: Recent literatures related to chondrocyte apoptosis were summarized and analyzed. During the process of osteoarthritis, changes in vascular endothelial growth factors in chondrocytes and regulatory effects of vascular endothelial growth factor and hypoxia-inducible factor on chondrocyte apoptosis were elaborated.
RESULTS AND CONCLUSION: Vascular endothelial growth factor promote the survival of chondrocytes by upregulating the expression of anti-apoptotic factors, and hypoxia-inducible factor can increase the activity of chondrocytes and extracellular matrix synthesis, which has become an important target for inhibition of chondrocyte apoptosis. However, the correlation between vascular endothelial growth factor and hypoxia-inducible factor remains to be further studied.

中国组织工程研究杂志出版内容重点：组织构建；骨细胞；软骨细胞；细胞培养；成纤维细胞；血管内皮细胞；骨质疏松；组织工程

Key words: Vascular Endothelial Growth Factors, Hypoxia-Inducible Factor 1, Chondrocytes, Apoptosis

CLC Number:

R318

Zhou Jian-lin, Fang Hong-song, Peng Hao, Deng Shuang, Weng Jin-qing, Liu Feng, Chen Sen, Zhou Guan-jin . Vascular endothelial growth factor and hypoxia-inducible factor suppress chondrocyte apoptosis[J]. Chinese Journal of Tissue Engineering Research, 2015, 19(29): 4705-4709.

Figures/Tables 1

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