The Role of Chondrocyte Hypertrophy and Senescence in Osteoarthritis Initiation and Progression

被引:399
作者
Rim, Yeri Alice [1 ]
Nam, Yoojun [1 ]
Ju, Ji Hyeon [1 ,2 ]
机构
[1] Catholic Univ Korea, Coll Med, Catholic iPSC Res Ctr, Seoul 06591, South Korea
[2] Catholic Univ Korea, Seoul St Marys Hosp, Inst Med Sci, Div Rheumatol,Dept Internal Med,Coll Med, Seoul 06591, South Korea
基金
新加坡国家研究基金会;
关键词
osteoarthritis; articular cartilage; chondrocyte; hypertrophy; senescence; GLYCATION END-PRODUCTS; HUMAN ARTICULAR CHONDROCYTES; CHONDROGENIC DIFFERENTIATION; CELLULAR SENESCENCE; GENE-EXPRESSION; CARTILAGE DEGENERATION; MMP-13; EXPRESSION; OXIDATIVE STRESS; II COLLAGEN; IN-VIVO;
D O I
10.3390/ijms21072358
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
070307 [化学生物学]; 071010 [生物化学与分子生物学];
摘要
Osteoarthritis (OA) is the most common joint disease that causes pain and disability in the adult population. OA is primarily caused by trauma induced by an external force or by age-related cartilage damage. Chondrocyte hypertrophy or chondrocyte senescence is thought to play a role in the initiation and progression of OA. Although chondrocyte hypertrophy and cell death are both crucial steps during the natural process of endochondral bone formation, the abnormal activation of these two processes after injury or during aging seems to accelerate the progression of OA. However, the exact mechanisms of OA progression and these two processes remain poorly understood. Chondrocyte senescence and hypertrophy during OA share various markers and processes. In this study, we reviewed the changes that occur during chondrocyte hypertrophy or senescence in OA and the attempts that were made to regulate them. Regulation of hypertrophic or senescent chondrocytes might be a potential therapeutic target to slow down or stop OA progression; thus, a better understanding of the processes is required for management.
引用
收藏
页数:15
相关论文
共 109 条
[1]
Elimination of BMP7 from the developing limb mesenchyme leads to articular cartilage degeneration and synovial inflammation with increased age [J].
Abula, Kahaer ;
Muneta, Takeshi ;
Miyatake, Kazumasa ;
Yamada, Jun ;
Matsukura, Yu ;
Inoue, Makiko ;
Sekiya, Ichiro ;
Graf, Daniel ;
Economides, Aris N. ;
Rosen, Vicki ;
Tsuji, Kunikazu .
FEBS LETTERS, 2015, 589 (11) :1240-1248
[2]
A complex secretory program orchestrated by the inflammasome controls paracrine senescence [J].
Acosta, Juan Carlos ;
Banito, Ana ;
Wuestefeld, Torsten ;
Georgilis, Athena ;
Janich, Peggy ;
Morton, Jennifer P. ;
Athineos, Dimitris ;
Kang, Tae-Won ;
Lasitschka, Felix ;
Andrulis, Mindaugas ;
Pascual, Gloria ;
Morris, Kelly J. ;
Khan, Sadaf ;
Jin, Hong ;
Dharmalingam, Gopuraja ;
Snijders, Ambrosius P. ;
Carroll, Thomas ;
Capper, David ;
Pritchard, Catrin ;
Inman, Gareth J. ;
Longerich, Thomas ;
Sansom, Owen J. ;
Aznar Benitah, Salvador ;
Zender, Lars ;
Gil, Jesus .
NATURE CELL BIOLOGY, 2013, 15 (08) :978-U221
[3]
Large-scale gene expression profiling reveals major pathogenetic pathways of cartilage degeneration in osteoarthritis [J].
Aigner, Thomas ;
Fundel, Katrin ;
Saas, Joachim ;
Gebhard, Pia M. ;
Haag, Jochen ;
Weiss, Tilo ;
Zien, Alexander ;
Obermayr, Franz ;
Zimmer, Ralf ;
Bartnik, Eckart .
ARTHRITIS AND RHEUMATISM, 2006, 54 (11) :3533-3544
[4]
Role of Chondrocytes in Cartilage Formation, Progression of Osteoarthritis and Cartilage Regeneration [J].
Akkiraju, Hemanth ;
Nohe, Anja .
JOURNAL OF DEVELOPMENTAL BIOLOGY, 2015, 3 (04) :177-192
[5]
The chondrocyte [J].
Archer, CW ;
Francis-West, P .
INTERNATIONAL JOURNAL OF BIOCHEMISTRY & CELL BIOLOGY, 2003, 35 (04) :401-404
[6]
Regulation of senescence associated signaling mechanisms in chondrocytes for cartilage tissue regeneration [J].
Ashraf, S. ;
Cha, B. -H. ;
Kim, J. -S. ;
Ahn, J. ;
Han, I. ;
Park, H. ;
Lee, S. -H. .
OSTEOARTHRITIS AND CARTILAGE, 2016, 24 (02) :196-205
[7]
Naturally occurring p16Ink4a-positive cells shorten healthy lifespan [J].
Baker, Darren J. ;
Childs, Bennett G. ;
Durik, Matej ;
Wijers, Melinde E. ;
Sieben, Cynthia J. ;
Zhong, Jian ;
Saltness, Rachel A. ;
Jeganathan, Karthik B. ;
Verzosa, Grace Casaclang ;
Pezeshki, Abdulmohammad ;
Khazaie, Khashayarsha ;
Miller, Jordan D. ;
van Deursen, Jan M. .
NATURE, 2016, 530 (7589) :184-+
[8]
TGF-BETA-1 PREVENTS HYPERTROPHY OF EPIPHYSEAL CHONDROCYTES - REGULATION OF GENE-EXPRESSION FOR CARTILAGE MATRIX PROTEINS AND METALLOPROTEASES [J].
BALLOCK, RT ;
HEYDEMANN, A ;
WAKEFIELD, LM ;
FLANDERS, KC ;
ROBERTS, AB ;
SPORN, MB .
DEVELOPMENTAL BIOLOGY, 1993, 158 (02) :414-429
[9]
Ageing and zonal variation in post-translational modification of collagen in normal human articular cartilage - The age-related increase in non-enzymatic glycation affects biomechanical properties of cartilage [J].
Bank, RA ;
Bayliss, MT ;
Lafeber, FPJG ;
Maroudas, A ;
Tekoppele, JM .
BIOCHEMICAL JOURNAL, 1998, 330 :345-351
[10]
Beaupré GS, 2000, J REHABIL RES DEV, V37, P145