Understanding how damage is caused in tendon disease
Disease - Tendonitis
Lead applicant - Mr Neal L Millar
Organisation - University of Glasgow
Type of grant - Project Grant
Status of grant - Active
Amount of the original award - £231,473.90
Start date - 1 January 2017
Reference - 21346
Public Summary
What are the aims of this research?
Disorders of the soft tissue can often affect tendons and are a very common form of musculoskeletal condition in the UK. Current therapies are not always effective, however the events which occur following tendon damage are not fully understood which is essential in finding effective treatments. This study aims to understand the role of the molecule, HMGB1 in tendon damage.
Why is this research important?
Tendons are the thick fibrous cords of dense connective tissue that attach muscles to bone. As such, tendons play a critical role in nearly every musculoskeletal activity - from standing to running to writing. Research into tendon diseases lags far behind other areas of the musculoskeletal system. Previous work by this research group looked at how small inflammatory molecules (cytokines) could cause change the structure of tendons and cause them to be weaker. Understanding the process of tendon injury is vital to finding a way to prevent and reverse tendon damage. HMGB1 is a protein which plays a role in a variety of responses to inflammation and in different diseases. When a tendon is damaged lots of small molecules are released into the joint, including HMGB1. Understanding how these molecules affect the breakdown of the tendon is important for discovering new targets for therapy. This group want to understand how HMGB1 is involved in tendon degeneration and try to block or reverse this process by altering the amount of HMGB1 in unhealthy tendons.
How will the findings benefit patients?
Current therapies available for tendon damage are not always effective. Understanding the processes involved in the damage of tendons can help identify potential new treatments for tendon damage.