Scientists Discover Key Proteins That Can Control Risk of Osteoarthritis

scientists discover key proteins that can control risk of osteoarthritis

Millions of Americans develop osteoarthritis as they age. Osteoarthritis is one of the most common type of arthritis among older people. A research at the Scripps Research Institute (TSRI) reveals why the risk of developing osteoarthritis increases with age. This study opened doors to finding novel and better treatment approaches in treating osteoarthritis and maintaining healthy joints. This study has identified FoxO proteins that are primarily responsible for maintaining healthy cells in the joint cartilages.

Martin Lotz, MD, professor and senior study author at TSRI explained that these FoxO proteins are responsible for controlling gene expression that is necessary for maintaining healthy cells. Therefore, drugs that can enhance the function and expression of FoxO genes can prevent development of osteoarthritis in people as they age. This could also lead to better treatment approaches for treating osteoarthritis patients.

Previous researches conducted by the same team revealed that as people age, the levels of FoxO proteins reduce significantly. Lotz and his team also observed that people with osteoarthritis have less gene expression for autophagy. Autophagy is a process wherein the cell recycles and consumes its own damaged parts to remain healthy.

The scientists used FoxO-deficient mouse models to observe how these proteins affect the joint cartilages with time. The mice whose FoxO coding genes have been knocked-out, showed significant joint cartilage degeneration as compared to the control mice. The FoxO deficient mice also showed severe osteoarthritis after an injury. Also, these were more prone to cartilage damage while running on a treadmill.


The research found out that the FoxO deficient mice had problems in their autophagy mechanisms and also were unable to prevent cell damage by oxidants. These mice also did not produce enough lubricin, which is a protein that generally protects cartilage damage due to friction and aging. This less amount of lubricin protein caused damage in the joint cartilage of the knee known as superficial zone. All these observations pointed out clearly that without proper function of these FoxO genes, there is significant inflammation and decreased cell autophagy.

The researchers used several genetic techniques to increase expression of the FoxO proteins in osteoarthritis patients. Surprisingly, the levels of protective genes and lubricin reverted to normal. The researchers plan further research to develop novel molecules that can enhance expression of FoxO proteins and test their efficacy in the osteoarthritis experimental models.

This study was recently published in the journal Science Translational Medicine.