Abstract
A recent article has revealed the potential of a subtype of voltage-gated sodium channel as a metabolic regulator and therapeutic target in osteoarthritis (OA). Functional Nav1.7 expression was identified in human OA-associated chondrocytes and shown in several genetic mouse models to promote disease progression. Thus, targeting and modulating it, including pharmacologically, could represent a previously unexplored avenue for developing therapeutic interventions to manage the disease. This study further highlights the need to understand the chondrocyte “channelome” more completely to unravel the diverse roles of ion channels in cartilage homeostasis and their clinical potential.
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