Dickkopf-1在强直性脊柱炎病理过程中作用研究进展
摘要
Dickkopf-1(Dkk-1)是Wnt信号路径的天然抑制因子,通过抑制Wnt信号传导通路影响骨化活动。体内Dkk-1血清水平降低、与Dkk-1受体的黏附功能下降或Dkk-1功能受损均可降低Dkk-1对Wnt信号传导通路的抑制作用,促进细胞内β-连环蛋白水平升高并活化,从而调节成骨细胞分化和倾向于骨生成,最终使强直性脊柱炎患者形成关节强直。强直性脊柱炎的炎症本身不受Dkk-1影响,且可以诱导Dkk-1的表达。
引文
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[14]Jun G,Minlin L,Dehong Y,et al.Suppression of Wntsignaling by Dkk-1 attenuates PTH-mediated stromal cellresponse and new bone formation[J].Cell Metab,2010,11(2):161-171.
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[17]Lories R J,Derese I,De Bari C,et al.Evidence for uncouplingof inflammation and joint remodeling in a mouse model ofspondylarthritis[J].Arthritis Rheum,2007,56(2):489-497.
[18]Sieper J,Appel H,Braun J,et al.Critical appraisal ofassessment of structural damage in ankylosing spondylitis:implications for treatment outcomes[J].Arthritis Rheum,2008,58(3):649-656.
[19]Maksymowych W P,Chiowchanwisawakit P,Clare T,et al.Inflammatory lesions of the spine on magnetic resonanceimaging predict the development of new syndesmophytes inankylosing spondylitis:evidence of a relationship betweeninflammation and new bone formation[J].Arthritis Rheum,2009,60(1):93-102.
[2]Van der Heijde D,Landewe R,Baraliakos X,et al.Radiographic findings following two years of infliximab therapyin patients with ankylosing spondylitis[J].Arthritis Rheum,2008,58(10):3063-3070.
[3]Bodine P V,Komm B S.Wnt signaling and osteoblastogenesis[J].Rev Endocr Metab Disord,2006,7(1/2):33-39.
[4]Glinka A,Wu W,Delius H,et al.Dickkopf-1is a member of anew family of secreted proteins and functions in head induction[J].Nature,1998,391(6665):357-362.
[5]Oyama T,Yamada Y,Hata K,et al.Further upregulation ofbeta-catenin/Tcf transcription is involved in the development ofmacroscopic tumors in the colon of ApcMin/+mice[J].Carcinogenesis,2008,29(3):666-672.
[6]Bafico A,Liu G,Yaniv A,et al.Novel mechanism of Wntsignalling inhibition mediated by Dickkopf-1interaction withLRP6[J].Nat Cell Biol,2001,3(7):683-686.
[7]Daoussis D,Andonopoulos A P,Liossis S N.Wnt pathway andIL-17:novel regulators of joint remodeling in rheumaticdiseases.Looking beyond the RANK-RANKL-OPG axis[J].Semin Arthritis Rheum,2010,39(5):369-383.
[8]Diarra D,Stolina M,Polzer K,et al.Dickkopf-1is a masterregulator of joint remodeling[J].Nat Med,2007,13(2):156-163.
[9]Peifer M,Polakis P.Wnt signaling in oncogenesis andembryogenesis:a look outside the nucleus[J].Science,2000,287(5458):1606-1609.
[10]Li J,Sarosi I,Cattley R C,et al.Dkk1-mediated inhibition ofWnt signaling in bone results in osteopenia[J].Bone,2006,39(4):754-766.
[11]MacDonald B T,Joiner D M,Oyserman S M,et al.Bone massis inversely proportional to Dkk1levels in mice[J].Bone,2007,41(3):331-339.
[12]Kwon S R,Lim M J,Suh C H,et al.Dickkopf-1level is lowerin patients with ankylosing spondylitis than in healthy peopleand is not influenced by anti-tumor necrosis factor therapy[J].Rheumatol Int,2012,32(8):2523-2527.
[13]Uderhardt S,Diarra D,Katzenbeisser J,et al.Blockade ofDickkopf-1induces fusion of sacroiliac joints[J].Ann RheumDis,2010,69(3):592-597.
[14]Jun G,Minlin L,Dehong Y,et al.Suppression of Wntsignaling by Dkk-1 attenuates PTH-mediated stromal cellresponse and new bone formation[J].Cell Metab,2010,11(2):161-171.
[15]Daoussis D,Liossis S N,Solomou E E,et al.Evidence thatDkk-1is dysfunctional in ankylosing spondylitis[J].ArthritisRheum,2010,62(1):150-158.
[16]Morvan F,Boulukos K,Clement-Lacroix P,et al.Deletion ofa single allele of the Dkk1gene leads to an increase in boneformation and bone mass[J].J Bone Miner Res,2006,21(6):934-945.
[17]Lories R J,Derese I,De Bari C,et al.Evidence for uncouplingof inflammation and joint remodeling in a mouse model ofspondylarthritis[J].Arthritis Rheum,2007,56(2):489-497.
[18]Sieper J,Appel H,Braun J,et al.Critical appraisal ofassessment of structural damage in ankylosing spondylitis:implications for treatment outcomes[J].Arthritis Rheum,2008,58(3):649-656.
[19]Maksymowych W P,Chiowchanwisawakit P,Clare T,et al.Inflammatory lesions of the spine on magnetic resonanceimaging predict the development of new syndesmophytes inankylosing spondylitis:evidence of a relationship betweeninflammation and new bone formation[J].Arthritis Rheum,2009,60(1):93-102.