Tendon problems such as Achilles pain, tennis elbow, swimmer’s shoulder and jumper’s knee affect many young athletes and older people. A research team led by Jess Snedeker and Katrien De Bock at ETH Zurich identified a central molecular driver: part of the HIF1 protein that acts as a transcription factor and controls gene activity in tendon cells.
To test causality, the researchers used experiments in mice and analysed human tendon tissue from surgeries. In mice, permanent activation of HIF1 produced tendon disease even without overloading. When HIF1 was switched off in tendons, the mice did not develop disease even with overload. These results show that elevated HIF1 can trigger tendinopathy.
Higher HIF1 caused pathogenic remodelling of tendon: more crosslinks formed in the collagen fibres, making tendons more brittle and reducing their mechanical function. Blood vessels and nerves also grew into the tissue, which may explain the pain. The team says early treatment is important because HIF1 damage can accumulate and become irreversible; advanced cases may need surgical removal of the diseased tendon.
Difficult words
- tendinopathy — disease or pain in a tendon
- transcription factor — protein that controls gene activity
- crosslink — a chemical bond between collagen fibrescrosslinks
- overload — too much physical load or stressoverloading
- remodelling — change in tissue structure or organization
- irreversible — cannot be changed back to original state
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Discussion questions
- Have you or someone you know had tendon pain? How did it affect daily activities or sports?
- What treatments or actions might help early tendon problems before surgery becomes necessary?
- How could athletes reduce the risk of tendon disease related to overload?
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