Laboratorio de Psicoinmunología, Instituto Nacional de Psiquiatría Ramón de la Fuente Muñiz, Colonia San Lorenzo Huipulco, Tlalpan, Ciudad de México, 14370, México.
Departamento de Inmunología, Escuela Nacional de Ciencias Biológicas, Instituto Politécnico Nacional, Miguel Hidalgo, Ciudad de México, México.
Mol Brain. 2024 May 26;17(1):29. doi: 10.1186/s13041-024-01102-9.
Fibromyalgia (FM) is a chronic condition that causes widespread pain, fatigue, and other symptoms that significantly affect quality of life. The underlying mechanisms of fibromyalgia involve both the immune system and the central nervous system. It has been proposed that changes in multiple ascending and descending pathways in the central nervous system may contribute to increased pain sensitivity in individuals with this condition. Recent research has identified S100 proteins as a new area of interest in fibromyalgia studies. These proteins are a group of small molecular weight proteins involved in inflammation and various functions inside and outside of cells, and they may play a critical role in the development and progression of FM. Although S100B has been the most studied in FM patients, other studies have reported that S100A7, S100A8, S100A9, and S100A12 may also be useful as potential biomarkers or for a deeper understanding of FM pathophysiology. The potential role of S100 proteins in the pathophysiology of fibromyalgia could be mediated by RAGE and TLR4, which signal through JNK, ERK, and p38 to activate AP-1 and NF-κB and induce the release of proinflammatory cytokines, thereby producing the inflammation, fatigue, and chronic pain characteristic of fibromyalgia. To gain new perspectives on targeted therapeutic approaches, it is crucial to understand how S100 proteins could impact the pathophysiology of fibromyalgia. This review examines the potential role of S100 proteins in fibromyalgia and their impact on improving our comprehension of the condition, as well as facilitating further research on this interesting topic.
纤维肌痛症(FM)是一种慢性疾病,会导致广泛的疼痛、疲劳和其他症状,严重影响生活质量。纤维肌痛症的潜在机制涉及免疫系统和中枢神经系统。有人提出,中枢神经系统中多个上行和下行通路的变化可能导致这种情况下的疼痛敏感性增加。最近的研究确定 S100 蛋白是纤维肌痛症研究的一个新领域。这些蛋白质是一组参与炎症和细胞内外各种功能的小分子质量蛋白,它们在 FM 的发展和进展中可能起着关键作用。虽然 S100B 在 FM 患者中研究最多,但其他研究报告称,S100A7、S100A8、S100A9 和 S100A12 也可能作为潜在的生物标志物或更深入了解 FM 病理生理学有用。S100 蛋白在纤维肌痛症病理生理学中的潜在作用可能通过 RAGE 和 TLR4 介导,它们通过 JNK、ERK 和 p38 信号传递来激活 AP-1 和 NF-κB,并诱导促炎细胞因子的释放,从而产生纤维肌痛症的炎症、疲劳和慢性疼痛特征。为了从新的角度了解靶向治疗方法,了解 S100 蛋白如何影响纤维肌痛症的病理生理学至关重要。这篇综述探讨了 S100 蛋白在纤维肌痛症中的潜在作用及其对改善我们对该疾病的理解的影响,并促进了对这一有趣主题的进一步研究。