Tendon pain is a problem that affects millions of people, from professional athletes to ordinary adults who simply stay active.
Conditions such as Achilles tendon pain, tennis elbow, swimmer’s shoulder, and jumper’s knee can make everyday movements difficult and painful.
Tendons are strong bands of tissue that connect muscles to bones and allow the body to move.
Every time you walk, lift, throw, or jump, your tendons transfer the force from your muscles to your skeleton. Because they handle such heavy loads, they are especially vulnerable to damage when they are used too much without enough rest.
Doctors call long-lasting tendon problems tendinopathies. These conditions often develop slowly when small injuries build up over time. At first, a person may feel only mild discomfort after exercise. But if the strain continues, the tendon can become weak, stiff, and painful even during simple activities.
Many people try rest, ice, or physical therapy, which can help in early stages. However, in severe cases these treatments may not work well, leaving patients with ongoing pain and limited movement. Scientists have been trying to understand why tendons sometimes fail to heal properly and why the damage can become permanent.
A research team from ETH Zurich and Balgrist University Hospital has now identified a key factor that may explain how tendon disease develops. They focused on a protein called HIF1, which helps cells respond when oxygen levels are low.
This protein normally plays an important role in helping tissues adapt to stress. However, the new study shows that when HIF1 becomes too active inside tendon tissue, it can actually trigger harmful changes that lead to disease.
To investigate this, researchers performed experiments in mice and also examined human tendon tissue collected during surgeries. In some mice, the scientists kept HIF1 permanently switched on. These animals developed tendon problems even without heavy physical strain.
In other mice, the protein was turned off specifically in tendon tissue. Surprisingly, these mice did not develop tendon disease even when their tendons were overloaded. This clear difference showed that HIF1 was not just present during tendon damage but was directly causing it.
The team also found that high levels of HIF1 changed the structure of the tendon itself. Tendons are made mostly of collagen fibers, which provide strength and flexibility. When HIF1 was too active, extra chemical links formed between these fibers, making the tendon stiffer and more brittle.
This reduces its ability to stretch and absorb force, increasing the risk of tears and pain. In addition, the researchers observed increased growth of blood vessels and nerve fibers inside the damaged tendon. This may explain why tendinopathy can be so painful, as more nerves are present to transmit pain signals.
These findings highlight the importance of early treatment. In young athletes especially, tendon pain is often ignored until it becomes severe.
Over time, damage caused by abnormal HIF1 activity can accumulate and become difficult or impossible to reverse. At that stage, physical therapy may no longer help, and surgery to remove damaged tissue may be the only option.
In reviewing the study, the discovery of HIF1 as a main driver of tendon disease is significant because it shifts the focus from simple overuse to deeper biological processes. It suggests that tendon injuries are not just mechanical problems but also involve changes inside cells.
This insight could lead to new treatments that target the molecular causes rather than only relieving symptoms. However, developing such therapies will be challenging because HIF1 also plays important roles in other parts of the body. Blocking it completely could cause unwanted side effects.
Future research will likely focus on finding ways to control this protein only in tendon tissue or to target other molecules that work with it. If successful, these efforts could lead to treatments that prevent tendon damage from becoming chronic and allow people to recover more fully.
Until then, the study reinforces a simple but important message: listening to early warning signs of tendon pain and allowing time for recovery may be the best way to protect long-term joint health.
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The study is published in Science Translational Medicine.
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