Inhibition of CD38 by apigenin limits injury-induced osteoarthritis development and associated pain in mice

Abstract

Purpose: Joint injury is a primary risk factor for development of osteoarthritis (OA). Degeneration of articular cartilage is a core OA disease feature. We have recently discovered that decline of NAD+, an intermediary metabolite that serves as a cofactor for numerous enzymes involved in cellular energy metabolism, is associated with increased expression and activity of CD38, the main NADase, in human knee chondrocyte and cartilage of OA and aged donors and in chondrocytes stimulated with IL-1β.