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Abstract：
Tendinitis, characterized by the inflammation of tendons, poses significant challenges in both diagnosis and treatment due to its multifaceted etiology and complex pathophysiology. This study aimed to dissect the molecular mechanisms underlying tendinitis, with a particular focus on inflammasome-related genes and their interactions with the immune system. Through comprehensive gene expression analysis and bioinformatics approaches, we identified distinct expression profiles of inflammasome genes, such as NLRP6, NLRP1, and MEFV, which showed significant correlations with immune checkpoint molecules, indicating a pivotal role in the inflammatory cascade of tendinitis. Additionally, MYD88 and CD36 were found to be closely associated with HLA family molecules, underscoring their involvement in immune response modulation. Contrary to expectations, chemokines exhibited minimal correlation with inflammasome genes, suggesting an unconventional inflammatory pathway in tendinitis. Transcription factors like SP110 and CREB5 emerged as key regulators of inflammasome genes, providing insight into the transcriptional control mechanisms in tendinitis. Furthermore, potential therapeutic targets were identified through the DGidb database, highlighting drugs that could modulate the activity of inflammasome genes, offering new avenues for targeted tendinitis therapy. Our findings elucidate the complex molecular landscape of tendinitis, emphasizing the significant role of inflammasomes and immune interactions, and pave the way for the development of novel diagnostic and therapeutic strategies.
摘要：
肌腱炎,以肌腱发炎为特征，由于其多方面的病因和复杂的病理生理学，在诊断和治疗方面都提出了重大挑战。本研究旨在剖析肌腱炎的分子机制。特别关注炎症相关基因及其与免疫系统的相互作用。通过全面的基因表达分析和生物信息学方法，我们确定了不同的炎症基因表达谱，例如NLRP6、NLRP1和MEFV，与免疫检查点分子显著相关，表明在肌腱炎的炎症级联反应中起关键作用。此外,发现MYD88和CD36与HLA家族分子密切相关，强调他们参与免疫应答调节。与预期相反,趋化因子与炎症体基因的相关性最小，提示肌腱炎的非常规炎症途径。转录因子如SP110和CREB5作为炎症体基因的关键调节因子，深入了解肌腱炎的转录控制机制。此外，通过DGidb数据库确定了潜在的治疗靶点，强调可以调节炎性体基因活性的药物，为有针对性的肌腱炎治疗提供新的途径。我们的发现阐明了肌腱炎的复杂分子景观，强调炎性体和免疫相互作用的重要作用，并为开发新的诊断和治疗策略铺平道路。
