ESPE Yearbook of Paediatric Endocrinology

To read the full abstract: The FASEB Journal 2019;33:12680–12695.

These authors conditionally deleted the IGF1 receptor gene (IGF1R) in tenocytes using a tamoxifen-inducible Cre-recombinase system and then stimulated plantaris tendon growth in adult mice via mechanical loading. Mice that lacked IGF1R in their tenocytes showed reduced cell proliferation and tendon growth in response to mechanical loading. These studies indicate that IGF1 signaling is required for postnatal tendon growth.

When longitudinal bones grow, so do the adjacent tendons. We don’t know much about tendons. They are a dense connective tissue that transmits force from muscle to bone during mechanical loading. Their extracellular matrix (ECM) is composed mostly of type I and type III collagen, elastin, and proteoglycans. Tendon fibroblasts (‘tenocytes’) are responsible for the synthesis, organization, and maintenance of the ECM. In response to high stress repetitive mechanical loading, such as during resistance exercise, tendons adapt by undergoing hypertrophy.

The authors hypothesized and showed that IGF1 signaling is required for normal tendon growth in response to mechanical loading, by regulating collagen synthesis and cell proliferation. Without IGF1 signaling, tendons were smaller and did not adapt normally. IGF1 may even become a new target for treating tendon injuries in humans.