[1] Aigner T, Hemmel M, Neureiter D, et al. Apoptotic cell death is not a widespread phenomenon in normal aging and osteoarthritis human articular knee cartilage: a study of proliferation, programmed cell death (apoptosis), and viability of chondrocytes in normal and osteoarthritic human knee cartilage [J]. Arthritis Rheum, 2001,44(6): 1304-1312.
[2] Horton WE Jr, Feng L, Adams C. Chondrocyte apoptosis in development, aging and disease [J]. Matrix Biol, 1998,17(2): 107-115.
[3] Kühn K, D’Lima DD, Hashimoto S, et al. Cell death in cartilage[J]. Osteoarthritis Cartilage, 2004,12(1): 1-16.
[4] Aigner T, Kim HA, Roach HI. Apoptosis in osteoarthritis[J]. Rheum Dis Clin North Am, 2004,30(3): 639-653.
[5] Vignon E, Arlot M, Patricot LM, et al. The cell density of human femoral head cartilage [J]. Clin Orthop Relat Res, 1976,(121): 303-308.
[6] Taniguchi N, Caramés B, Ronfani L, et al. Aging-related loss of the chromatin protein HMGB2 in articular cartilage is linked to reduced cellularity and osteoarthritis [J]. Proc Natl Acad Sci U S A, 2009,106(4): 1181-1186.
[7] Martin JA, Buckwalter JA. Telomere erosion and senescence in human articular cartilage chondrocytes [J]. J Gerontol A Biol Sci Med Sci, 2001,56(4): B172-B179.
[8] Hayflick L. Intracellular determinants of cell aging [J]. Mech Ageing Dev, 1984,28(2-3): 177-185.
[9] Campisi J. Senescent cells, tumor suppression, and organismal aging: good citizens, bad neighbors [J]. Cell, 2005,120(4): 513-522.
[10] Itahana K, Campisi J, Dimri GP. Mechanisms of cellular senescence in human and mouse cells [J]. Biogerontology, 2004,5(1): 1-10.
[11] Dai SM, Shan ZZ, Nakamura H, et al. Catabolic stress induces features of chondrocyte senescence through overexpression of caveolin 1: possible involvement of caveolin 1-induced down-regulation of articular chondrocytes in the pathogenesis of osteoarthritis [J]. Arthritis Rheum, 2006,54(3): 818-831.
[12] Freund A, Patil CK, Campisi J. p38MAPK is a novel DNA damage response-independent regulator of the senescence-associated secretory phenotype [J]. EMBO J, 2011,30(8): 1536-1548.
[13] Coppé JP, Patil CK, Rodier F, et al. Senescence-associated secretory phenotypes reveal cell-nonautonomous functions of oncogenic RAS and the p53 tumor suppressor [J]. PLoS Biol, 2008,6(12): 2853-2868.
[14] Coppé JP, Desprez PY, Krtolica A, et al. The senescence-associated secretory phenotype: the dark side of tumor suppression [J]. Annu Rev Pathol, 2010,5: 99-118.
[15] Coppé JP, Rodier F, Patil CK, et al. Tumor suppressor and aging biomarker p16(INK4a) induces cellular senescence without the associated inflammatory secretory phenotype [J]. J Biol Chem, 2011,286(42): 36396-36403.
[16] Rodier F, Coppé JP, Patil CK, et al. Persistent DNA damage signalling triggers senescence-associated inflammatory cytokine secretion [J]. Nat Cell Biol, 2009,11(8): 973-979.
[17] Shen M, Luo Y, Niu Y, et al. 1,25(OH)2D deficiency induces temporomandibular joint osteoarthritis via secretion of senescence-associated inflammatory cytokines [J]. Bone, 2013, 55(2): 400-409.
[18] Mizushima N, Levine B, Cuervo AM, et al. Autophagy fights disease through cellular self-digestion [J]. Nature, 2008,451(7182): 1069-1075.
[19] Tooze SA, Yoshimori T. The origin of the autophagosomal membrane [J]. Nat Cell Biol, 2010,12(9): 831-835.
[20] Gamerdinger M, Hajieva P, Kaya AM, et al. Protein quality control during aging involves recruitment of the macroautophagy pathway by BAG3 [J]. EMBO J, 2009,28(7): 889-901.
[21] Haigis MC, Yankner BA. The aging stress response [J]. Mol Cell, 2010,40(2): 333-344.
[22] Caramés B, Hasegawa A, Taniguchi N, et al. Autophagy activation by rapamycin reduces severity of experimental osteoarthritis [J]. Ann Rheum Dis, 2012,71(4): 575-581.
[23] Lotz MK, Caramés B. Autophagy and cartilage homeostasis mechanisms in joint health, aging and OA [J]. Nat Rev Rheumatol, 2011,7(10): 579-587.
[24] Lotz M, Caramés B. Autophagy: a new therapeutic target in cartilage injury and osteoarthritis [J]. J Am Acad Orthop Surg, 2012,20(4): 261-262.
[25] Caramés B, Taniguchi N, Otsuki S, et al. Autophagy is a protective mechanism in normal cartilage, and its aging-related loss is linked with cell death and osteoarthritis [J]. Arthritis Rheum, 2010,62(3): 791-801.
[26] Sasaki H, Takayama K, Matsushita T, et al. Autophagy modulates osteoarthritis-related gene expression in human chondrocytes [J]. Arthritis Rheum, 2012,64(6): 1920-1928.
[27] Caramés B, Taniguchi N, Seino D, et al. Mechanical injury suppresses autophagy regulators and pharmacologic activation of autophagy results in chondroprotection [J]. Arthritis Rheum, 2012,64(4): 1182-1192.
[28] Fukui N, Ikeda Y, Ohnuki T, et al. Regional differences in chondrocyte metabolism in osteoarthritis: a detailed analysis by laser capture microdissection [J]. Arthritis Rheum, 2008,58(1): 154-163.
[29] Sandell LJ, Aigner T. Articular cartilage and changes in arthritis. An introduction: cell biology of osteoarthritis [J]. Arthritis Res, 2001,3(2): 107-113.
[30] Aigner T, Zhu Y, Chansky HH, et al. Reexpression of type IIA procollagen by adult articular chondrocytes in osteoarthritic cartilage [J]. Arthritis Rheum, 1999,42(7): 1443-1450.
[31] Visco DM, Johnstone B, Hill MA, et al. Immunohistochemical analysis of 3-B-(-) and 7-D-4 epitope expression in canine osteoarthritis [J]. Arthritis Rheum, 1993,36(12): 1718-1725.
[32] Hudelmaier M, Glaser C, Hohe J, et al. Age-related changes in the morphology and deformational behavior of knee joint cartilage [J]. Arthritis Rheum, 2001,44(11): 2556-2561.
[33] Ding C, Cicuttini F, Scott F, et al. Association between age and knee structural change: a cross sectional MRI based study [J]. Ann Rheum Dis, 2005,64(4): 549-555.
[34] Verzijl N, Bank RA, TeKoppele JM, et al. AGEing and osteoarthritis: a different perspective [J]. Curr Opin Rheumatol, 2003,15(5): 616-622.
[35] Garg S, Syngle A, Vohra K. Efficacy and tolerability of advanced glycation end-products inhibitor in osteoarthritis: a randomized, double-blind, placebo-controlled study [J]. Clin J Pain, 2013,29(8):717-724.
[36] Yamabe S, Hirose J, Uehara Y, et al. Intracellular accumulation of advanced glycation end products induces apoptosis via endoplasmic reticulum stress in chondrocytes [J]. FEBS J, 2013,280(7):1617-1629.
[37] Chen AC, Temple MM, Ng DM, et al. Induction of advanced glycation end products and alterations of the tensile properties of articular cartilage [J]. Arthritis Rheum, 2002,46(12): 3212-3217.
[38] Verzijl N, DeGroot J, Ben ZC, et al. Crosslinking by advanced glycation end products increases the stiffness of the collagen network in human articular cartilage: a possible mechanism through which age is a risk factor for osteoarthritis [J]. Arthritis Rheum, 2002,46(1): 114-123.
[39] Vos PA, DeGroot J, Barten-van Rijbroek AD, et al. Elevation of cartilage AGEs does not accelerate initiation of canine experimental osteoarthritis upon mild surgical damage [J]. J Orthop Res, 2012,30(9): 1398-1404.
[40] Goodwin W, McCabe D, Sauter E, et al. Rotenone prevents impact-induced chondrocyte death [J]. J Orthop Res, 2010,28(8): 1057-1063.
[41] Liu JT, Guo X, Ma WJ, et al. Mitochondrial function is altered in articular chondrocytes of an endemic osteoarthritis, Kashin-Beck disease [J]. Osteoarthritis Cartilage, 2010,18(9): 1218-1226.
[42] Scott JL, Gabrielides C, Davidson RK, et al. Superoxide dismutase downregulation in osteoarthritis progression and end-stage disease [J]. Ann Rheum Dis, 2010,69(8): 1502-1510.
[43] Naik E, Dixit VM. Mitochondrial reactive oxygen species drive proinflammatory cytokine production [J]. J Exp Med, 2011,208(3): 417-420.
[44] Jallali N, Ridha H, Thrasivoulou C, et al. Vulnerability to ROS-induced cell death in ageing articular cartilage: the role of antioxidant enzyme activity [J]. Osteoarthritis Cartilage, 2005,13(7): 614-622.
[45] Aigner T, Fundel K, Saas J, et al. Large-scale gene expression profiling reveals major pathogenetic pathways of cartilage degeneration in osteoarthritis [J]. Arthritis Rheum, 2006,54(11): 3533-3544. |