Үе мөчний мөгөөрсөн эдийг нөхөн төлжүүлэх боломжтойг эрдэмтэд тогтоов

One of the most disappointing and most relatable parts of aging is the experience of a joint no longer doing what it’s supposed to do: knees that hurt when you bend down, shoulders that clunk.

The general assumption for decades has been that once the cartilage in a joint has broken down, it can’t be regrown.

But now, scientists at Stanford University think they’ve found the switch that’s been holding this process back, after tracing the loss of age-related cartilage to a single protein.

When they blocked it in mice, old, worn-down cartilage started to thicken again.

The protein is an enzyme called 15-PGDH, and it’s already been extensively linked to aging.

It’s known that, as we get older, 15-PGDH becomes more abundant and interferes with the molecules that repair tissue and reduce inflammation.

That link to aging is what led the Stanford team to question whether the same protein might be driving osteoarthritis – a condition that’s caused by the breakdown of cartilage collagen, resulting in pain and inflammation in the joint.

In old mice, blocking 15-PGDH thickened cartilage that had already worn away.

And in young mice with a fresh injury, it prevented the arthritis that usually follows. To test this, the researchers recreated the mouse equivalent of an anterior cruciate ligament (ACL) tear and then blocked 15-PGDH. The osteoarthritis that you’d normally expect to see after such an injury didn’t occur.

What’s especially interesting is that in this study, stem cells didn’t seem to play a part.

Chondrocytes, the adult cells that already build and maintain cartilage, were actually able to become healthier once 15-PGDH was reduced.

“This is a new way of regenerating adult tissue, and it has significant clinical promise for treating arthritis due to aging or injury,” Stanford University stem cell biologist Helen Blau said in November last year when the research was first published.

“We were looking for stem cells, but they are clearly not involved. It’s very exciting.”

As you can see below, the aged mice with cartilage with 15-PGDH blocked (far right) had cartilage that appeared similar to young, healthy cartilage (left).

It wasn’t only mice. The team also tested the approach on human cartilage taken from people undergoing knee replacement surgery and saw the same pattern: tissue that became stiffer and less inflamed after treatment.

“The mechanism is quite striking and really shifted our perspective about how tissue regeneration can occur,” explained orthopedic scientist Nidhi Bhutani.

“It’s clear that a large pool of already existing cells in cartilage are changing their gene expression patterns. And by targeting these cells for regeneration, we may have an opportunity to have a bigger overall impact clinically.”

This one potential therapy is exciting enough on its own, but it’s just one contender in what’s becoming a genuinely crowded race to end osteoarthritis.

The US government’s Advanced Research Projects Agency for Health (ARPA-H) has put forward more than US$100 million to fast-track several separate teams chasing the same basic goal through different biology, under a program called NITRO.

Two years in, those teams have already regenerated both cartilage and bone in animals, and the next milestone is people.

One of the recipients of the grants, the University of Colorado Boulder, made headlines earlier this year when researchers unveiled a slow-release drug-delivery system that is injected into the damaged joint and coaxes the body’s own cartilage and bone cells to repair themselves in just a few weeks.

The tests so far have all been in animal models, but they’ve now spun out their research into a company called Renovare Therapeutics, which is focused on clinical trials in humans.

“In two years, we were able to go from a moonshot idea to developing these therapies to demonstrating that they reverse osteoarthritis in animals,”saidchemical and biological engineer Stephanie Bryant, from the University of Colorado Boulder in a press release earlier this year.

“Our goal is not just to treat pain and halt progression, but to end this disease.”

A team at Columbia University has also received an ARPA-H grant, but they’ve taken quite a different approach: 3D-printing a living human knee scaffold seeded with stem cells that dissolves as the body regrows its own cartilage and bone around it.

“NITRO, ARPA-H’s first program, was launched with the question: What if we could make our joints heal themselves?” said program manager Ross Uhrich.

“Two years later, it’s not only possible, but quickly becoming a reality.”

In the meantime, there may be a potential treatment that’s already widely in use.

A 2026 study found that semaglutide appears to protect joints – and it appears to do so via a mechanism that’s independent of easing pressure through weight loss.

The team from China and the US found that the drug reprograms the metabolism of cells that maintain healthy cartilage, allowing them to generate more energy.

In mice and humans with obesity and osteoarthritis, treatment with semaglutide reduced pain and decreased cartilage degeneration.

In mice, they included a control group that ate the same amount as the semaglutide-treated animals. Even with comparable weight changes, that control group did not receive the same cartilage protection, suggesting a weight-loss-independent effect on the joint itself.

While more research needs to be done, the fact that many people already take semaglutide means it’s something that can be studied further going forward.

Related: Experimental Drug Can Reverse Osteoarthritis in Weeks, Animal Research Shows

For the Stanford team, the next step will include a clinical trial.

That can be a long process, but a 15-PGDH blocker to combat muscle weakness has already been tested in a previous human trial and didn’t raise any red flags for health and safety, which should speed up the trial process for similar drugs.

“We are very excited about this potential breakthrough,”saidBlau.

“Imagine regrowing existing cartilage and avoiding joint replacement.”

The study was published in the journalScience.