Scientists at the University of Southern California have discovered a promising way to help aging joints heal and possibly slow down or reverse the effects of osteoarthritis, a common condition that affects millions of older adults.
The key to this new approach lies in a special protein called STAT3, which the researchers found can help cartilage cells regain their youth and function better.
Osteoarthritis is a type of arthritis that causes the cartilage and bones in joints to break down over time. This can lead to pain, stiffness, swelling, and limited movement. It usually affects people as they get older and is often the result of years of wear and tear on the joints.
While doctors can offer treatments to help manage the symptoms—like exercise, physical therapy, medications, or surgery—there is currently no cure.
In this new study, the researchers focused on how the cells that make cartilage age and what can be done to reverse those changes. They looked closely at how certain genes are turned on or off as we get older.
These patterns, which are part of a process called “epigenetic regulation,” control how cells function. Over time, aging changes these patterns in cartilage cells, making them less effective at keeping joints healthy.
The team created an “epigenetic clock” to measure how old cartilage cells are on a molecular level. Then, using a special chemical tool, they activated the STAT3 protein in these aging cells.
When STAT3 was turned on, it caused many important genes to become active again and helped return the aging cartilage cells to a more youthful state. In other words, STAT3 helped turn back the clock in these cells.
When the researchers turned off STAT3, the opposite happened—the clock ticked faster, and the cells began to show patterns seen in older cartilage. This made the cells less able to function and more likely to contribute to the progression of osteoarthritis.
The scientists also studied another protein called DNMT3B, which works closely with STAT3. They discovered that when STAT3 was inactive, DNMT3B encouraged the development of osteoarthritis in the knee joints of mice that had suffered joint injuries. These mice developed cartilage cells that looked young but didn’t function properly.
The scientists believe the cells were trying to repair the joint by becoming more like early-stage cells, but in doing so, they created faulty cartilage that didn’t work well in the long term.
This study is important because it suggests a new way to treat osteoarthritis. By activating STAT3 in the right way, it may be possible to help joints heal without causing inflammation, which can make arthritis worse. This could lead to treatments that encourage real regeneration of joint tissue, offering hope to people with chronic joint problems.
The research was led by Dr. Denis Evseenko and published in the journal Aging Cell. While more work is needed before this can be tested in humans, the discovery opens up exciting possibilities for future therapies that could help people maintain healthier joints as they age.
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