Yale researchers have pinpointed a potential drug target that could ease joint degeneration associated with osteoarthritis, a debilitating condition affecting up to 30 million people in the United States. The study, published on January 3 in the journal Nature, highlights the urgent need for therapies preventing joint breakdown in osteoarthritis, as current treatments mainly focus on pain relief and lifestyle changes.
The research, led by Chuan-Ju Liu and Stephen G. Waxman at Yale School of Medicine, identifies sodium channels, specifically Nav1.7, as key players in transmitting pain signals. While these channels were previously known for their role in “excitable” cells within muscles, the nervous system, and the heart, the study reveals their presence in non-excitable cells responsible for collagen production and joint maintenance.
Osteoarthritis, the most prevalent form of arthritis, results from cartilage breakdown between joints, commonly occurring in the hands, hips, and knees. By deleting Nav1.7 genes from collagen-producing cells, the researchers significantly reduced joint damage in mouse models of osteoarthritis. Additionally, drugs inhibiting Nav1.7, such as carbamazepine (currently used to treat epilepsy and trigeminal neuralgia), demonstrated substantial protection against joint damage in mice.
Stephen G. Waxman commented on the study’s significance, stating, “The function of sodium channels in non-excitable cells has been a mystery.” The findings open new possibilities for disease-modifying treatments, offering hope for addressing the underlying causes of osteoarthritis.
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