The authors point out that after surgery for large or massive tears, patients often sustain recurrent tears and, even if the repair remains intact, have poor muscle function. These poor results may be related to irreversible atrophy and fatty infiltration of the rotator cuff muscles.
They developed a small animal model of rotator cuff tears and used this model to identify the ways in which cuff tears affect the associated muscle. They found an intracellular signaling pathway (Akt/mTOR) that appears to be important in regulating muscle mass in normal muscle also has a central role in the development of muscle atrophy and fatty infiltration. Inhibiting this pathway decreases the development of fatty infiltration.
In a rat model the authors demonstrated that transecting the supraspinatus, infraspinatus, and teres minor tendons created muscle atrophy and fatty infiltration along with muscle fibrosis, changes that were increased by denervation.
They used MRI to quantitate muscle atrophy and fatty infiltration and to evaluate the role of Akt/mTOR and of transforming growth factor-beta (TGF-β) in the development of these changes.
Finally, the authors investigated the cellular source of fibroblasts and adipocytes that infiltrate the muscle causing irreversible changes, suggesting that these cells arise from endothelial lineage stem cells. They are searching for a stimulus or small molecule inhibitors to drive these cells to make muscle instead of fibrous tissue and fat, avoiding atrophy and fatty infiltration.
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