Why the study?
Rotator cuff tear frequently triggers muscle degeneration characterised by muscle atrophy, fatty infiltration, and fibrosis, but underlying transcriptional changes in the supraspinatus muscle remained to be revealed.
Single-nucleus transcriptomics reveals the plasticity of muscle cells and specific transcriptional changes in response to rotator cuff tear, offering potential therapeutic targets.
May identify targets to limit atrophy after rotator cuff tear; extends myonuclear trajectory mapping while leaving open clinical validation.
Rotator cuff tear (RCT) is the primary cause of shoulder pain and disability and frequently trigger muscle degeneration characterised by muscle atrophy, fatty infiltration and fibrosis. Single‐nucleus RNA sequencing (snRNA‐seq) was used to reveal the transcriptional changes in the supraspinatus muscle after RCT. Supraspinatus muscles were obtained from patients with habitual shoulder dislocation ( n = 3) and RCT ( n = 3). In response to the RCT, trajectory analysis showed progression from normal myonuclei to ANKRD1 + myonuclei, which captured atrophy‐and fatty infiltration‐related regulons (KLF5, KLF10, FOSL1 and BHLHE40). Transcriptomic alterations in fibro/adipogenic progenitors (FAPs) and muscle satellite cells (MuSCs) have also been studied. By predicting cell–cell interactions, we observed communication alterations between myofibers and muscle‐resident cells following RCT. Our findings reveal the plasticity of muscle cells in response to RCT and offer valuable insights into the molecular mechanisms and potential therapeutic targets of RCT.
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Sun et al. (2024) studied this question.
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