Researchers at Yale University found a potential drug target that could help ease joint damage in osteoarthritis, a painful condition affecting around 30 million people in the U.S. Traditional treatments like pain relievers, exercise, and weight loss help manage symptoms, but there’s a need for therapies that can stop the joint breakdown in osteoarthritis.
Particular proteins called sodium channels in cell membranes create electrical signals in muscles, nerves, and the heart. Yale researcher Stephen G. Waxman previously highlighted the role of one sodium channel, Nav1.7, in transmitting pain signals. Now, the labs of Chuan-Ju Liu and Waxman at Yale School of Medicine discovered that Nav1.7 channels are also in non-excitable cells that produce collagen and support joint maintenance.
Osteoarthritis is a common arthritis resulting from cartilage breakdown between joints, often affecting the hands, hips, and knees. In a recent study, scientists removed Nav1.7 genes from cells producing collagen, reducing joint damage in mice with osteoarthritis. They also found that drugs blocking Nav1.7, like carbamazepine for epilepsy and neuralgia, protected mice from joint damage.
Waxman said “that the function of sodium channels in non-excitable cells has been a mystery. This new study shows how small numbers of sodium channels can powerfully regulate the behavior of non-excitable cells.”
A research scientist in the Liu laboratory and first author of the study, Wenyu Fu, said, “The findings open new avenues for disease-modifying treatments.”
In conclusion, the study’s promising findings suggest that the epilepsy drug carbamazepine, known for blocking Nav1.7 genes, holds the potential to slow down joint degeneration in osteoarthritis. These insights offer a hopeful direction for repurposing existing medications to address the urgent need for effective therapies in managing and preventing joint damage associated with this prevalent and debilitating condition.
Journal reference:
- Fu, W., Vasylyev, D., Bi, Y. et al. Nav1.7 as a chondrocyte regulator and therapeutic target for osteoarthritis. Nature. DOI:10.1038/s41586-023-06888-7.