Molecular mechanisms of cell death in intervertebral disc degeneration (Review)

被引:237
作者
Zhang, Fan [1 ,2 ]
Zhao, Xueling [2 ]
Shen, Hongxing [1 ]
Zhang, Caiguo [3 ]
机构
[1] Second Mil Med Univ, Changhai Hosp, Dept Orthoped, Shanghai 200433, Peoples R China
[2] Kunming Med Univ, Affiliated Hosp 1, Dept Orthoped, Kunming 650032, Yunnan, Peoples R China
[3] Univ Colorado, Sch Med, Dept Biochem & Mol Genet, Aurora, CO 80045 USA
关键词
apoptosis; autophagy; nucleus pulposus; annulus fibrosus; cartilage endplate; NUCLEUS PULPOSUS CELLS; END-PLATE CHONDROCYTES; FAS-MEDIATED APOPTOSIS; SIGNALING PATHWAYS; MITOCHONDRIAL PATHWAY; INHIBITS APOPTOSIS; SERUM DEPRIVATION; AUTOPHAGY; EXPRESSION; CANCER;
D O I
10.3892/ijmm.2016.2573
中图分类号
R-3 [医学研究方法]; R3 [基础医学];
学科分类号
1001 ;
摘要
Intervertebral discs (IVDs) are complex structures that consist of three parts, namely, nucleus pulposus, annulus fibrosus and cartilage endplates. With aging, IVDs gradually degenerate as a consequence of many factors, such as microenvironment changes and cell death. Human clinical trial and animal model studies have documented that cell death, particularly apoptosis and autophagy, significantly contribute to IVD degeneration. The mechanisms underlying this phenomenon include the activation of apoptotic pathways and the regulation of autophagy in response to nutrient deprivation and multiple stresses. In this review, we briefly summarize recent progress in understanding the function and regulation of apoptosis and autophagy signaling pathways. In particular, we focus on studies that reveal the functional mechanisms of these pathways in IVD degeneration.
引用
收藏
页码:1439 / 1448
页数:10
相关论文
共 96 条
[1]   ACUTE MECHANICAL INJURY OF THE HUMAN INTERVERTEBRAL DISC: LINK TO DEGENERATION AND PAIN [J].
Alkhatib, B. ;
Rosenzweig, D. H. ;
Krock, E. ;
Roughley, P. J. ;
Beckman, L. ;
Steffen, T. ;
Weber, M. H. ;
Ouellet, J. A. ;
Haglund, L. .
EUROPEAN CELLS & MATERIALS, 2014, 28 :98-111
[2]   The expression and role of non-canonical (PKC) signaling in nucleus pulposus cell metabolism [J].
Arai, Fumiyuki ;
Hiyama, Akihiko ;
Sakai, Daisuke ;
Yokoyama, Katsuya ;
Mochida, Joji .
JOURNAL OF ORTHOPAEDIC RESEARCH, 2012, 30 (09) :1478-1485
[3]   Mechanical stress-induced apoptosis of endplate chondrocytes in organ-cultured mouse intervertebral discs -: An ex vivo study [J].
Ariga, K ;
Yonenobu, K ;
Nakase, T ;
Hosono, N ;
Okuda, S ;
Meng, WX ;
Tamura, Y ;
Yoshikawa, H .
SPINE, 2003, 28 (14) :1528-1533
[4]   The relationship between apoptosis of endplate chondrocytes and aging and degeneration of the intervertebral disc [J].
Ariga, K ;
Miyamoto, S ;
Nakase, T ;
Okuda, S ;
Meng, WX ;
Yonenobu, K ;
Yoshikawa, H .
SPINE, 2001, 26 (22) :2414-2420
[5]   Regulated Cell Death: Signaling and Mechanisms [J].
Ashkenazi, Avi ;
Salvesen, Guy .
ANNUAL REVIEW OF CELL AND DEVELOPMENTAL BIOLOGY, VOL 30, 2014, 30 :337-356
[6]   Directing cancer cells to self-destruct with pro-apoptotic receptor agonists [J].
Ashkenazi, Avi .
NATURE REVIEWS DRUG DISCOVERY, 2008, 7 (12) :1001-1012
[7]   Repair, regenerative and supportive therapies of the annulus fibrosus: achievements and challenges [J].
Bron, Johannes Leendert ;
Helder, Marco N. ;
Meisel, Hans-Jorg ;
Royen, Barend J. Van ;
Smit, Theodoor H. .
EUROPEAN SPINE JOURNAL, 2009, 18 (03) :301-313
[8]   Occurrence and regional distribution of apoptosis in scoliotic discs [J].
Chen, BH ;
Fellenberg, J ;
Wang, HL ;
Carstens, C ;
Richter, W .
SPINE, 2005, 30 (05) :519-524
[9]   Hypoxia facilitates the survival of nucleus pulposus cells in serum deprivation by down-regulating excessive autophagy through restricting ROS generation [J].
Chen, Jiang-Wei ;
Ni, Bin-Bin ;
Zheng, Xin-Feng ;
Li, Bo ;
Jiang, Sheng-Dan ;
Jiang, Lei-Sheng .
INTERNATIONAL JOURNAL OF BIOCHEMISTRY & CELL BIOLOGY, 2015, 59 :1-10
[10]   The Responses of Autophagy and Apoptosis to Oxidative Stress in Nucleus Pulposus Cells: Implications for Disc Degeneration [J].
Chen, Jiang-Wei ;
Ni, Bin-Bin ;
Li, Bo ;
Yang, Yue-Hua ;
Jiang, Sheng-Dan ;
Jiang, Lei-Sheng .
CELLULAR PHYSIOLOGY AND BIOCHEMISTRY, 2014, 34 (04) :1175-1189