Muscle ‘control centre’ may improve injury recovery in old age

Cells that help manage muscle repair have been identified, offering potential new ways to treat age-related muscle loss and improve healing in older adults.

Researchers have discovered that a type of cell known as fibro-adipogenic progenitors (FAPs) plays a key role in coordinating the body’s muscle regeneration process after injury.

The study found that these cells act like construction managers, working with immune cells to ensure damaged muscle is repaired efficiently.

Researchers from Aarhus University and Steno Diabetes Center Aarhus made the discovery while studying how different cell types communicate during healing.

Associate professor Jean Farup of the Department of Biomedicine at Aarhus University, said: “Our primary finding is the pronounced inter-cellular communication between fibro-adipogenic progenitors (FAPs) and immune cells, which helps ensure the function of immune cells and thereby support muscle regeneration.”

The research showed that FAPs communicate directly with macrophages – immune cells responsible for removing damaged tissue and supporting the healing process – to coordinate muscle reconstruction.

Farup said: “FAPs are thus a kind of coordinator that lives in the house and knows how it should be rebuilt and communicates with the various craftsmen necessary for the reconstruction.”

One of the study’s most surprising findings was that FAPs produce the signalling substance complement C3 directly within muscle tissue.

Until now, it had been thought that this substance was only produced in the liver before entering circulation.

This local production of complement C3 was shown to be crucial for regulating the inflammation required for effective muscle healing.

The discovery could open new avenues for treating muscle loss in elderly and chronically ill patients.

Long-term inflammation is known to be linked to conditions such as type 2 diabetes, cardiovascular disease and cancer.

Farup said: “We know that inflammation plays a significant role both in relation to muscle regeneration and in connection with muscle mass loss in patients and elderly people.

“Our new insight therefore provides new opportunities to regulate inflammation with, for example, medicine that affects FAPs.”

The team now plans to explore how this mechanism operates in chronic inflammatory conditions that contribute to muscle deterioration.