Scientists Crack Code Behind Tennis Elbow and Achilles Pain

Millions of people suffering from tennis elbow, Achilles pain, and jumper's knee may finally have hope for better treatment thanks to a groundbreaking discovery from Swiss researchers.

Scientists at ETH Zurich and Balgrist University Hospital have identified HIF1, a protein that doesn't just show up in damaged tendons but actually drives the disease process. The finding answers a question that has puzzled doctors for years: why do these painful overuse injuries resist treatment in so many patients?

"Tendons must withstand powerful loads, with all the forces of our muscles being concentrated to the relatively thin tendons that transmit these forces," explains Jess Snedeker, professor of orthopaedic biomechanics at ETH Zurich. These conditions, called tendinopathies, are among the most common reasons people visit orthopedic specialists.

Previous studies had noticed higher HIF1 levels in damaged tendons but couldn't prove whether the protein caused the problem or simply appeared alongside it. The research team solved this puzzle through clever experiments in mice and human tendon cells.

When researchers kept HIF1 permanently active in mice, the animals developed tendon disease even without heavy use. In contrast, mice with HIF1 switched off stayed healthy even when their tendons faced intense strain.

The experiments revealed exactly how HIF1 damages tendons. The protein causes harmful crosslinks to form in collagen fibers, making tendons brittle and mechanically weaker. It also triggers blood vessels and nerves to grow into tendon tissue, which likely explains the chronic pain patients experience.

Why This Inspires

This discovery matters most for young athletes who often struggle with these injuries when treatment could still work. "Our study shows that it's important to treat tendon problems early," says Snedeker, noting that damage from HIF1 can become irreversible over time.

Greta Moschini, the doctoral student who led the study, emphasizes the practical hope this research brings. Right now, severe cases often require surgery to remove diseased tendons. Understanding HIF1's role gives scientists a target for developing medicines that could prevent or reverse the damage.

The team isn't promising quick fixes. Professor Katrien De Bock notes that simply switching off HIF1 throughout the body would cause side effects, since the protein serves important functions in other organs. The more promising path involves studying the biochemical processes around HIF1 to find better drug targets.

That's exactly what the researchers plan to do next. Their work could identify other molecules controlled by HIF1 that are safer targets for treatment, potentially helping millions avoid chronic pain and surgery.

Better treatments for these stubborn injuries are on the horizon.