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SPARC – a genetic predisposition factor for tendon and ligament injuries 

Tendons transfer great forces between muscles and bones – a human Achilles tendon could be used to pull a small car. Without the protein “SPARC”, however, they are poorly developed and tear easily under load. In humans, a defective SPARC gene variant means that those affected more often end up in hospital with torn tendons and ligaments. 

“SPARC is usually produced by tendon cells and secreted into the extracellular matrix”, explained Andreas Traweger, who works at the Institute for Tendon and Bone Regeneration at the Paracelsus Medical University in Salzburg. 

Together with Minghao Zheng from The University of Western Australia and professor Jiang Qin at Nanjing University (China), he examined the Achilles tendons of mice without SPARC. They were less developed than in normal mice, withstanding less traction at the bone attachment and tore more often after walking on the treadmill. 

“In our study, we were able to show that the extracellular matrix is weaker when this protein is missing,” says Traweger: “As a result, the embedded cells perceive loads such as stretching to a greater extent”. This causes tendons to deteriorate: the matrix, including protein fibers, is broken down and inflammation occurs. 

The findings are clinically relevant in two respects, explained the expert: “On the one hand, athletes could be examined to see whether they are exposed to an increased risk of a tendon rupture.” Moreover, he is currently working on a follow-up project with the aim to determine whether the administration of SPARC protein can promote the tendon healing. 

Read the full study here: Load-induced regulation of tendon homeostasis by SPARC, a genetic predisposition factor for tendon and ligament injuries.