Osteoarthritis is the most common form of arthritis, a chronic inflammatory disease that is characterized by the degradation of the cartilage found between the joints – especially those of the hands, hips and knees – and which, when deteriorated, contributes to the occurrence of osteoarthritis. frictions. A team of scientists at Yale University (USA) has now discovered that a drug used to treat epilepsy could help stop joint degeneration associated with osteoarthritis.
Osteoarthritis is the most common rheumatic disease, since, according to data from the Spanish Society of Rheumatology, around 30% of people over 40 years of age suffer from osteoarthritis in one of their joints; Specifically, about 242 million people suffer from this disease around the world, and in Spain there are about seven million affected.
The treatment of this disease is based on the administration of analgesics and improvements in lifestyle habits, such as weight loss and physical exercise, with the aim of relieving stiffness and pain, but it is necessary to find therapeutic options that help prevent fractures. Yale researchers have identified a drug target that may reduce joint degeneration associated with this condition.
A therapeutic goal to reduce joint damage
Specialized proteins known as sodium channels found in cell membranes are known to produce electrical impulses in “excitable” cells within the muscles, nervous system and heart. And in previous research, Yale’s Stephen G. Waxman identified the key role of one sodium channel in particular, called Nav1.7, in transmitting pain signals.
Now, the labs of Chuan-Ju Liu and Waxman, both at Yale School of Medicine, have discovered that the same Nav1.7 channels are also present in non-excitable cells that produce collagen and help maintain the body’s joints. In the new research, its authors eliminated the Nav1.7 genes from these collagen-producing cells and significantly decreased joint damage in two mouse models of osteoarthritis.
Drugs to treat epilepsy and trigeminal neuralgia used to block Nav1.7 provided substantial protection against joint damage in mice
The results have been published in the journal Nature and have also shown that drugs used to block Nav1.7 (including carbamazepine, a sodium channel blocker currently used to treat epilepsy and trigeminal neuralgia) They also provided substantial protection against joint damage in mice.
“The function of sodium channels in non-excitable cells has been a mystery,” said Waxman. “This new study offers a window into how a small number of sodium channels can powerfully regulate the behavior of non-excitable cells.” “The findings open new avenues for disease-modifying treatments,” concludes Wenyu Fu, a researcher in Liu’s laboratory and first author of the study.
