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Research advance on intervertebral disc degeneration and cell death / 中国骨伤
China Journal of Orthopaedics and Traumatology ; (12): 673-678, 2015.
Article in Chinese | WPRIM | ID: wpr-240966
ABSTRACT
Intervertebral disc degeneration is considered as a primary cause of clinical low back pain, however the molecular mechanism is not clear yet. Recently, researches on the molecular basis of intervertebral disc degeneration have become a hotspot. The special structure and biomechanics properties of the disc contribute to its propensity toward degeneration. Intervertebral disc degeneration is associated with the changes of the cytological behavior,including the increase in cell death and the degradation of extracellular matrix. However, the mechanism of cell death including cell apoptosis and autophagy in intervertebral disc degeneration remains unclear. Further study on the molecular mechanism of intervertebral disc degeneration is the foundation of improving and treating the intervertebral disc degeneration in the future. Although some progresses are made in the aspect of biological study, the biological environment of intervertebral disc itself is still a challenge for the development of biological treatment. This article is to review the latest advance on the biological characteristics of normal intervertebral disc and the cell death in the process of the intervertebral disc degeneration.
Subject(s)
Full text: Available Index: WPRIM (Western Pacific) Main subject: Cell Death / Apoptosis / Cell Biology / Extracellular Matrix / Intervertebral Disc Degeneration / Intervertebral Disc / Metabolism Limits: Animals / Humans Language: Chinese Journal: China Journal of Orthopaedics and Traumatology Year: 2015 Type: Article

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Full text: Available Index: WPRIM (Western Pacific) Main subject: Cell Death / Apoptosis / Cell Biology / Extracellular Matrix / Intervertebral Disc Degeneration / Intervertebral Disc / Metabolism Limits: Animals / Humans Language: Chinese Journal: China Journal of Orthopaedics and Traumatology Year: 2015 Type: Article