Calcific tendinopathy (CT), developed due to calcium hydroxyapatite deposition in the rotator cuff tendon, mostly affects women in their 40 s and 50 s and causes severe shoulder pain. However, the molecular basis of its pathogenesis and appropriate treatment methods are largely unknown. In this study, we identified 202 differentially expressed genes (DEGs) between calcific and adjacent normal tendon tissues of rotator cuff using RNA sequencing-based transcriptome analysis. The DEGs were highly enriched in extracellular matrix (ECM) degradation and inflammation-related processes. Further, matrix metalloproteinase 9 (MMP9) and matrix metalloproteinase 13 (MMP13), two of the enzymes associated with ECM degradation, were found to be highly upregulated 25.85- and 19.40-fold, respectively, in the calcific tendon tissues compared to the adjacent normal tendon tissues. Histopathological analyses indicated collagen degradation and macrophage infiltration at the sites of calcific deposit in the rotator cuff tendon. Our study acts as a foundation that may help in better understanding of the pathogenesis associated with CT, and thus in better management of the disease.

钙化肌腱病（CT）是由于羟基磷灰石钙沉积在肩袖肌腱中而引起的，主要在40多岁和50多岁时影响女性，并导致严重的肩部疼痛。但是，其发病机理的分子基础和适当的治疗方法尚不清楚。在这项研究中，我们使用基于RNA测序的转录组分析方法，确定了肩袖钙化和邻近正常肌腱组织之间的202个差异表达基因（DEG）。DEG在细胞外基质（ECM）降解和炎症相关过程中高度富集。此外，发现与ECM降解相关的两种酶基质金属蛋白酶9（MMP9）和基质金属蛋白酶13（MMP13）分别被上调25.85和19.40倍，与邻近的正常肌腱组织相比，钙化肌腱组织中的钙离子含量更高。组织病理学分析表明，在肩袖肌腱钙化沉积部位胶原蛋白降解和巨噬细胞浸润。我们的研究奠定了基础，可能有助于更好地了解与CT相关的发病机制，从而更好地控制疾病。