Parvin Afroza, Sharma Ashish Ranjan, Hasan Md Ashraful, Sharma Garima, Shawan Mohammad Mahfuz Ali Khan, Seo Eun Min, Hasan Md Mahmudul, Lee Sang-Soo
Department of Biochemistry and Molecular Biology, Jahangirnagar University, Dhaka, Bangladesh.
Department of Pharmacology and Therapeutics, University of Manitoba, Winnipeg, MB, Canada.
Front Immunol. 2025 Sep 12;16:1633318. doi: 10.3389/fimmu.2025.1633318. eCollection 2025.
Ankylosing spondylitis (AS) is a chronic autoimmune disorder that primarily affects young people. Although genetic and environmental factors have been implicated in the pathogenesis of AS, the etiology of this condition remains unclear. Observations indicate that individuals possessing the human leukocyte antigen (HLA)-B27 allele exhibit elevated risk factors, as any mutation within this gene could potentially result in the development of AS in the future. However, it is interesting to note that many AS patients do not carry this gene, inferring the involvement of other genetic and nongenetic factors in the development of the disease. As the exact mechanisms remain unknown, no target-specific treatments exist to cure AS. Nonetheless, some treatment regimens have been devised to alleviate AS symptoms. This review thoroughly examines the molecular mechanisms implicated in AS, encompassing insights into the significance of pivotal biomarkers, such as extracellular matrix metabolites, immune cell dynamics, gut microbiota interactions, the Wnt signaling pathway, and its inhibitors. Furthermore, a thorough evaluation of the different mouse models used in AS research has been reviewed, which is crucial for understanding disease pathways and assessing treatment methods. In addition, significant progress in developing effective treatment strategies for AS, along with drugs available for treatment and ongoing clinical trials, has been summarized. A comprehensive understanding of experimental mouse models, along with insights into molecular mechanisms and biomarkers for AS, could aid researchers and physicians in discovering new treatment strategies for this challenging condition.
强直性脊柱炎（AS）是一种主要影响年轻人的慢性自身免疫性疾病。尽管遗传和环境因素与AS的发病机制有关，但这种疾病的病因仍不清楚。观察表明，携带人类白细胞抗原（HLA）-B27等位基因的个体表现出较高的风险因素，因为该基因内的任何突变都可能在未来导致AS的发生。然而，有趣的是，许多AS患者并不携带该基因，这表明其他遗传和非遗传因素也参与了该疾病的发展。由于确切机制仍然未知，目前尚无针对AS的特异性治疗方法。尽管如此，已经设计了一些治疗方案来缓解AS症状。本综述全面研究了与AS相关的分子机制，包括对关键生物标志物的重要性的见解，如细胞外基质代谢物、免疫细胞动态、肠道微生物群相互作用、Wnt信号通路及其抑制剂。此外，还对AS研究中使用的不同小鼠模型进行了全面评估，这对于理解疾病途径和评估治疗方法至关重要。此外，还总结了在开发AS有效治疗策略方面取得的重大进展，以及可用的治疗药物和正在进行的临床试验。对实验小鼠模型的全面了解，以及对AS分子机制和生物标志物的见解，可能有助于研究人员和医生为这种具有挑战性的疾病发现新的治疗策略。
