The current progress in understanding the molecular functions and mechanisms of visfatin in osteoarthritis

Abstract

Osteoarthritis, (OA), also known as degenerative arthritis or degenerative joint disease, is the most common form of arthritis, affecting millions of people worldwide. It is a group of mechanical abnormalities involving degradation of the joints and occurs when the protective cartilage (articular cartilage) on the ends of bones such as the knees, hips and fingers abrades over time. It mainly affects the whole joint structure, including the articular cartilage, subchondral bone and synovial tissue. Extensive work has been done in the past decades to investigate the cellular mechanism of this disease. However, to date, it is still poorly understood, and there is no effective treatment. Recently, both in vitro and in vivo studies have confirmed adipokines play critical roles during OA development. Among these, leptin and adiponectin have been well investigated, whereas the effect of the novel adipokine, visfatin, on OA still needs to be revealed. Therefore, in this short review, we will focus on visfatin and summarize the current progress in the research on its role in OA development.

Visfatin increases ICAM-1 expression and monocyte adhesion in human osteoarthritis synovial fibroblasts by reducing miR-320a expression

“…Previous findings of higher visfatin concentrations in synovial fluid from OA patients compared with healthy synovial fluid [ 21 , 22 ] were confirmed in this study. Our analysis of records from the GEO database also found higher visfatin levels in inflammatory synovial tissue than in normal synovial tissue.…”

Low-grade inflammation as a key mediator of the pathogenesis of osteoarthritis

“…Several adipokines, such as leptin, adiponectin, resistin, visfatin, and nefastin-1, have context-dependent immunomodulatory properties 115,116 and can induce the production of inflammatory mediators and cartilage-degrading factors, leading to chondrocyte degradation and the development of OA 112,115,117–124 . Visfatin, for instance, the expression or enzyme activity level of which is regulated by IL-1β, hypoxia-inducible factor 2α (HIF-2α), and other interleukins, not only inhibits the phosphorylation of insulin receptor factors such as IRS1 and AKT, thus reducing proteoglycan production, but also increases the expression of MMPs, NGF, and PGE2, thereby aggravating OA 120 . Adipokines are also produced in the OA joint by infrapatellar fat pads, synovium, chondrocytes, osteoblasts, and osteoclasts 125,126 , which could additionally serve as local sources of other inflammatory mediators in the joint, such as neuropeptides and the classic inflammatory cytokines IL-1β, IL-6, and TNF 30 .…”

The Adipokine Network in Rheumatic Joint Diseases

“…Systemic visfatin levels are increased in OA patients compared to healthy controls [175,176] but serum levels are lower compared to chronic-inflammatory diseases such as RA. However, OASF respond to visfatin even at low concentrations with increased secretion of pro-inflammatory factors such as IL-8, MCP-1 and other chemokines [170].…”