Rotator Cuff Impingement Damages the Organelles of Tenocytes, Resulting in Excessive Tenocyte Apoptosis and Tendinopathy.

This article focuses on the role of mitochondrial dysfunction and endoplasmic reticulum (ER) stress in excessive apoptosis of tenocytes contributing to rotator cuff tendinopathy, using a mouse model of subacromial impingement. The study demonstrated that impingement induced significant biomechanical deterioration, histopathological changes, and elevated apoptosis in supraspinatus tendons, with peak effects observed at four weeks post-injury. Molecular analyses revealed upregulation of mitochondrial apoptotic markers (e.g., caspase-3, caspase-9) and ER stress mediators (e.g., caspase-12, CHOP), while transmission electron microscopy showed mitochondrial degeneration and ER dilation. These findings suggest a cooperative interaction between mitochondrial and ER pathways in tenocyte apoptosis, highlighting early organelle-level pathological changes that may inform future therapeutic strategies for tendinopathy.