+ Site Statistics
+ 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/RANK as key factors for osteoclast development and bone loss in arthropathies

RANKL/RANK as key factors for osteoclast development and bone loss in arthropathies

Advances in Experimental Medicine and Biology 649: 100-113

Osteoporosis or rheumatoid arthritis are bone diseases affecting hundreds of millions of people worldwide and thus pose a tremendous burden to health care. Ground-breaking discoveries made in basic science over the last decade shed light on the molecular mechanisms of bone metabolism and bone turnover. Thereby, it became possible over the past years to devise new and promising strategies for treating such diseases. In particular, three molecules, the receptor activator of NF-kappaB (RANK), its ligand RANKL and the decoy receptor of RANKL, osteoprotegerin (OPG), have been a major focus of scientists and pharmaceutical companies alike, since experiments using mice in which these genes have been inactivated unanimously established their pivotal role as central regulators ofosteoclast function. RANK(L) signaling not only activates a variety of downstream signaling pathways required for osteoclast development, but crosstalk with other signaling pathways also fine-tunes bone homeostasis both in normal physiology and disease. Consequently, novel drugs specifically targeting RANK-RANKL and their signaling pathways in osteoclasts are expected to revolutionize the treatment ofvarious bone diseases, such as cancer metastases, osteoporosis, or arthropathies.

(PDF emailed within 1 workday: $29.90)

Accession: 055333212

Download citation: RISBibTeXText

PMID: 19731623

Related references

Discovery of osteoclast differentiation factor, RANKL Inhibition of bone resorption by blocking RANKL-RANK signaling. Japanese Journal of Pharmacology 88(Supplement 1): 17P, 2002

Bone loss in the spondyloarthropathies: role of osteoclast, RANKL, RANK and OPG in the spondyloarthropathies. Advances in Experimental Medicine and Biology 649: 85-99, 2009

Human osteoclast formation and bone resorption by a mechanism independent of RANK/RANKL Role of IL-6 and IL-11. Journal of Bone & Mineral Research 16(Suppl 1): S381, September, 2001

Molecular pathways: osteoclast-dependent and osteoclast-independent roles of the RANKL/RANK/OPG pathway in tumorigenesis and metastasis. Clinical Cancer Research 18(2): 326-335, 2012

Retinoic acid increases proliferation of human osteoclast progenitors and inhibits RANKL-stimulated osteoclast differentiation by suppressing RANK. Plos One 5(10): E13305-E13305, 2011

Osteoclast formation in osteoclast precursor cell line RAW2647 is not correlated to OPG, RANK or RANKL expression, but is influenced by culture conditions. Journal of Bone & Mineral Research 16(Suppl 1): S506, September, 2001

Simulated rates of resorption during cancellous bone remodeling using Michaelis-Menten equations and the interactive effects of RANKL, RANK and OPG on osteoclast activity. Calcified Tissue International 72(4): 363, April, 2003

Association between osteoprotegerin (OPG), receptor activator of nuclear factor-kappaB (RANK), and RANK ligand (RANKL) gene polymorphisms and circulating OPG, soluble RANKL levels, and bone mineral density in Korean postmenopausal women. Menopause 14(5): 913-918, 2007

RANK, RANKL and osteoprotegerin in arthritic bone loss. Brazilian Journal of Medical and Biological Research 38(2): 161-170, 2005

Role of RANKL and RANK in bone loss and arthritis. Annals of the Rheumatic Diseases 61 Suppl 2: Ii32-Ii39, 2002

Factors regulating osteoclast formation in human tissues adjacent to peri-implant bone loss: expression of receptor activator NFkappaB, RANK ligand and osteoprotegerin. Biomaterials 25(4): 565-573, 2003

RANKL/RANK: from bone loss to the prevention of breast cancer. Open Biology 6(11): -, 2016

Decursin from Angelica gigas suppresses RANKL-induced osteoclast formation and bone loss. European Journal of Pharmacology 774: 34-42, 2016

Osteoclast precursors, RANKL/RANK, and immunology. Immunological Reviews 208: 19-29, 2005

Fatostatin, an SREBP inhibitor, prevented RANKL-induced bone loss by suppression of osteoclast differentiation. Biochimica et Biophysica Acta 1852(11): 2432-2441, 2015