EurekaMag.com logo
+ Site Statistics
References:
53,869,633
Abstracts:
29,686,251
+ Search Articles
+ Subscribe to Site Feeds
EurekaMag Most Shared ContentMost Shared
EurekaMag PDF Full Text ContentPDF Full Text
+ PDF Full Text
Request PDF Full TextRequest PDF Full Text
+ Follow Us
Follow on FacebookFollow on Facebook
Follow on TwitterFollow on Twitter
Follow on LinkedInFollow on LinkedIn

+ Translate

RANKL as a target molecule for treatment of joint destruction



RANKL as a target molecule for treatment of joint destruction



Clinical Calcium 17(4): 586-592



Rheumatoid arthritis (RA) is a chronic inflammatory disorder characterized progressive joint destruction. Recent studies have revealed an essential role of receptor activator of NF-kappaB ligand (RANKL) in bone destruction in RA, and therapeutics targeting RANKL has been attracting a great deal of attention.

(PDF emailed within 1 workday: $29.90)

Accession: 055333156

Download citation: RISBibTeXText

PMID: 17404489



Related references

Anti-RANKL treatment inhibits erosive joint destruction and lowers inflammation but has no effect on bone formation in the delayed-type hypersensitivity arthritis (DTHA) model. Arthritis Research & Therapy 18(): 28-28, 2016

The ratio of circulating osteoprotegerin to RANKL in early rheumatoid arthritis predicts later joint destruction. Arthritis and Rheumatism 54(6): 1772-1777, 2006

Osteoclast inhibitory lectin , RANKL and OPG expression at sites of inflammation and joint destruction in rheumatoid and collagen-induced arthritis. Journal of Bone & Mineral Research 16(Suppl 1): S305, September, 2001

Anti-RANKL antibody for the treatment of bone and cartilage destruction in rheumatoid arthritis. Clinical Calcium 25(12): 1787-1793, 2016

Gene therapy in rheumatoid arthritis: how to target joint destruction?. Arthritis Research 1(1): 5-9, 2000

An LFA-1 (alphaLbeta2) small-molecule antagonist reduces inflammation and joint destruction in murine models of arthritis. Journal of Immunology 184(7): 3917-3926, 2010

The osteoclast: a potential therapeutic target of bone and joint destruction in rheumatoid arthritis. Modern Rheumatology 11(3): 177-183, 2001

Construction of the control system of target molecule expression in Escherichia coli: application to a validation platform for bactericidal and bacteriostatic profiles due to suppression of a target molecule. Fems Microbiology Letters 331(2): 113-119, 2012

New method for analysis of target molecule in gastrointestinal carcinoma--from the choice of ATP7B as a target molecule for overcoming drug resistance through the development of an inhibitor against ATP7B. Nihon Shokakibyo Gakkai Zasshi 101(1): 18-26, 2004

Mammalian target of rapamycin signaling is crucial for joint destruction in experimental arthritis and is activated in osteoclasts from patients with rheumatoid arthritis. Arthritis and Rheumatism 62(8): 2294-2302, 2010

Osteopetrosis rescue upon RANKL administration to Rankl(-/-) mice: a new therapy for human RANKL-dependent ARO. Journal of Bone and Mineral Research 27(12): 2501-2510, 2013

It is said that elevated erythrocyte sedimentation rate and the elevation of C-reactive protein (CRP) may be indicators of continuing joint destruction in rheumatoid arthritis. What then is the explanation for joint destruction in some patients in whom there is no such apparent elevation of either the sedimentation rate of CRP?. British Journal of Rheumatology 29(2): 88-88, 1990

A novel therapeutic vaccine approach against RANKL that prevents pathological bone destruction. Clinical Calcium 15(7): 62-66, 2005

Regulation of bone destruction in rheumatoid arthritis through RANKL-RANK pathways. World Journal of Orthopedics 4(1): 1-6, 2013

Expression of RANKL and OPG mRNA in periodontal disease: possible involvement in bone destruction. International Journal of Molecular Medicine 11(1): 17-21, 2002