Autophagy genes associated with chondrocyte apoptosis: protection and balancing effects

doi:10.3969/j.issn.2095-4344.2015.20.022

Abstract

Abstract:

BACKGROUND: Autophagy can occur in chondrocytes under the low supply of nutrients. Different from necrosis and apoptosis, autophagy can make chondrocytes survive in insufficient supply of nutrients, which may be an important mechanism for the self-protection of chondrocytes.
OBJECTIVE: To review the mechanism and effect of autophagy gene to protect the articular cartilage and inhibit osteoarthritis.
METHODS: A computer-based search was perform in CNKI, Wanfang, PubMed to retrieve articles addressing autophagy gene and osteoarthritis published from January 2000 to January 2015. The keywords were “autophagy, osteoarthritis, articular cartilage, chondrocytes” in Chinese and “autophagy, osteoarthritis, beclin1, LC3” in English. Totally 269 articles were initially searched, and finally, 38 articles were included in result analysis.
RESULTS AND CONCLUSION: Apoptosis of damaged chondrocytes is the main mechanism of articular cartilage degeneration, which can further develop into osteoarthritis. The damage and death of cells is one of the important mechanisms of cartilage degeneration, thus, to prevent damaged chondrocyte apoptosis may help cartilage repair, thus alleviating the progression of osteoarthritis. Autophagy can inhibit damaged chondrocyte apoptosis, which changes the limitations of traditional treatments for osteoarthritis. However, the current research on autophagy genes associated with osteoarthritis is still at the primary stage, and further studies are needed on how to induce authopagy pathway in the cartilage, how to do the signal transduction and how to have an effect on the survival of chondrocytes.

Key words: Ostoarthritis, Autophagy, Genes, Chondrocytes

CLC Number:

R318

Liu Li-guo, Xu Chao, Yilihamu Tuoheti. Autophagy genes associated with chondrocyte apoptosis: protection and balancing effects[J]. Chinese Journal of Tissue Engineering Research, 2015, 19(20): 3231-3235.

Figures/Tables 1

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