Introduction: Advanced age increases the prevalence of rotator cuff tears and affects the success of repair surgeries. Cellular senescence is proposed as a key mechanism behind these age-related differences, likely due to contribution of the senescence-associated secretory phenotype (SASP). This state is linked to various age-related diseases, including rotator cuff injuries.
Materials And Methods: Rotator cuff muscle samples were obtained from young and aged patients undergoing surgery. Samples were processed for single-cell RNA sequencing (scRNA-seq) to analyze cellular differences. Cells were isolated and sequenced to identify different cell populations and their gene expression profiles.
Results: Six major cell populations were identified in rotator cuff muscle tissue, including fibroadipogenic progenitor (FAP) cells, satellite cells, endothelial cells, pericytes, macrophages, and T-cells. Aged FAPs showed higher expression of senescence markers and genes associated with fibrosis and inflammation. Younger FAPs had higher levels of extracellular matrix remodeling genes. Specifically, ATF3 - a senescence marker - was found to be elevated in aged FAPs. In silico analysis highlighted a potential role of ATF3 in regulating FAP differentiation.
Conclusions: Markers of cellular senescence are significantly elevated in older human rotator cuff tissue samples compared to young rotator cuff. Of specific interest is ATF3, a gene that has been previously implicated in regulating adipogenesis, which demonstrates a trend in to function in a protective capacity against the formation of fibrosis in computational analysis of our data.
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