Visfatin as a Potential Inflammatory Biomarker and Therapeutic Target in Osteoarthritis: A Narrative Review.

Abstract

Osteoarthritis (OA) is a common, chronic degenerative joint disease that leads to the progressive degeneration of articular cartilage, subchondral bone, and synovium. In short, it is characterized primarily by inflammation, cartilage breakdown, and subchondral bone remodeling leading to joint pain, stiffness, and severe functional limitations. OA pathogenesis results from complex reciprocal interactions between genetic, mechanical, and environmental factors that culminate in the activation of pro-inflammatory mediators such as Interleukin 1β (IL 1β) and Tumor Necrosis Factor alpha (TNF α), which stimulate Matrix Metalloproteinases (MMPs) and break down the cartilage extracellular matrix. Additionally, oxidative stress, mitochondrial dysfunction, and chondrocyte senescence play crucial roles in disease progression. Consequently, adipokines have become important contributors to OA pathophysiology, with special emphasis on visfatin. These molecules released from adipose tissue also represent a systemic proinflammatory signal, found at higher concentrations in OA synovial fluid, and contribute to cartilage degradation and worsening of clinical symptoms. Visfatin participates in various signaling pathways to further amplify inflammatory cascades and cartilage destruction. In this review, we explore the role of visfatin and its possible mechanisms contributing to the progression of OA.