[RANKL/RANK signaling in rheumatoid arthritis]

Yasunori Omata; Sakae Tanaka

[RANKL/RANK signaling in rheumatoid arthritis]

Clin Calcium. 2011 Aug;21(8):1175-80.

[Article in Japanese]

Authors

Yasunori Omata¹, Sakae Tanaka

Affiliation

¹ Department of Orthopaedic Surgery, The University of Tokyo, Japan.

PMID: 21814022

Abstract

Rheumatoid arthritis (RA) is a chronic inflammatory disease, which is induced by abundant inflammatory cytokines releasing from synovial fibroblasts and T lymphocytes. These cytokines differentiate monocyte-macrophage lineage cells to mature osteoclasts, which cause bone resorption and then joint destruction. RANKL is involved in the development of osteoclasts, cooperating with another key molecule, M-CSF. Indeed, RANKL is over-expressed in the synovium of RA. We summarize RANKL/RANK signaling in RA, including recent therapeutic topics.

Publication types

English Abstract
Review

MeSH terms

Arthritis, Rheumatoid / drug therapy
Arthritis, Rheumatoid / genetics*
Arthritis, Rheumatoid / metabolism
Bone Resorption
Cell Differentiation
Cytokines / physiology
Humans
Inflammation Mediators / physiology
Macrophage Colony-Stimulating Factor / metabolism
Macrophages / cytology
Molecular Targeted Therapy
Monocytes / cytology
Osteoclasts* / physiology
RANK Ligand / physiology*
Receptor Activator of Nuclear Factor-kappa B / physiology*
Signal Transduction / physiology*
Synovial Membrane / metabolism

Substances

Cytokines
Inflammation Mediators
RANK Ligand
Receptor Activator of Nuclear Factor-kappa B
TNFRSF11A protein, human
Macrophage Colony-Stimulating Factor