ArticleBMC musculoskeletal disorders2022
Characteristics of gene expression in frozen shoulder.
Article in BMC musculoskeletal disorders, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed.
- Shoulder and genetics: what orthopedic surgeons need to know.JSES reviews, reports, and techniques · 2026Review
- From inflammatory activation to fibrotic remodeling: the central role of macrophage heterogeneity in frozen shoulder.Frontiers in immunology · 2026Review
- Signaling pathway networks in frozen shoulder fibrosis: from inflammatory initiation to fibrotic progression.Frontiers in medicine · 2026Review
- Basic Science Research in Frozen Shoulder: Current Updates.Indian journal of orthopaedics · 2025Article
- Acupotomy Alleviates Capsular Fibrosis in Frozen Shoulder Rats by Modulating CCL2 to Inhibit Macrophage Recruitment and Suppress the Inflammatory Response.Journal of inflammation research · 2025Article
- SOX9: a key transcriptional regulator in organ fibrosis.Frontiers in pharmacology · 2025Review
- Drug Repurposing for Frozen Shoulder; a Bioinformatics Meta-Analysis.The archives of bone and joint surgery · 2025Article
- Relationship Between Metabolic Profile, Pain, and Functionality in Patients with Frozen Shoulder: A Cross-Sectional Study.Healthcare (Basel, Switzerland) · 2024Article
- Inferior glenohumeral joint capsule thickness in frozen shoulder via ultrasonography.JSES international · 2024Article
- Article
- Arthroscopic treatment for rotator cuff injury and frozen shoulder with concomitant rotator cuff injury: analysis of efficacy and factors influencing prognosis.American journal of translational research · 2024Article
- Causal relationships between systemic inflammatory cytokines and adhesive capsulitis: a bidirectional Mendelian randomization study.Frontiers in immunology · 2024Article
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Authors and funding
5 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundSevere frozen shoulder (FS) is often resistant to treatment and can thus result in long-term functional impairment. However, its etiology remains unknown. We hypothesized that gene expression of FS would vary by synovial location.
methodsThe synovial tissues of patients with FS were collected prospectively and analyzed for the expression of 19 genes. Synovial tissues from patients with rotator cuff tear (RCT) or shoulder instability (SI) were also analyzed as controls. A total of 10 samples were analyzed from each group. The specimens were arthroscopically taken from three different locations: rotator interval (RI), axillary recess (AX), and subacromial bursa (SAB). Total RNA was extracted from the collected tissues and was analyzed by real-time polymerase chain reaction for the following genes: matrix metalloproteinases (MMPs); tissue inhibitors of metalloproteinases (TIMPs); inflammatory cytokines (IL1B, TNF, and IL6); type I and II procollagen (COL1A1 and COL2A1); growth factors (IGF1 and TGFB1); neural factors (NGF and NGFR); SOX9; and ACTA2.
resultsSite-specific analysis showed that MMP13, IL-6, SOX9, and COL1A1 were increased in all three sites. Four genes (MMP3, MMP9, COL2A1, and NGFR) were increased in the AX, MMP3 in the RI, and NGFR in the SAB were increased in the FS group than in the RCT and SI groups. In the FS group, there was a correlation between the expression of genes related to chondrogenesis (MMP2, IGF1, SOX9, COL2A1, NGF, and NGFR) or fibrosis (MMP9, TGFB1, and COL1A1).
conclusionThe expression levels of numerous MMPs, pro-inflammatory cytokines, and collagen-related genes were increased in the FS group, suggesting that catabolic and anabolic changes have simultaneously occurred. In addition, genes related to chondrogenesis or fibrosis were highly expressed in the FS group, which might have affected the range of motion limitation of the shoulder. Compared to RI and SAB, the AX was the most common site of increased expression in FS. Analyzing the lower region of the shoulder joint may lead to the elucidation of the pathogenesis of FS.
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