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通过 VEXAS 综合征的视角理解骨髓增生异常和炎症:综述。

Understanding Myelodysplasia and Inflammation Through the Lense of VEXAS Syndrome: A Review.

机构信息

Department of Internal Medicine, Erasme Hospital, Brussels University Hospital, Université Libre de Bruxelles (ULB), Route de Lennik 808, 1070 Brussels, Belgium.

Department of Medicine, Division of Internal Medicine, Lausanne University Hospital (CHUV), University of Lausanne, 1005 Lausanne, Switzerland.

出版信息

Cells. 2024 Nov 15;13(22):1890. doi: 10.3390/cells13221890.

Abstract

VEXAS syndrome, a monogenic X-linked disorder resulting from mutations in the UBA1 gene, has emerged as a key model for unraveling the links between systemic inflammatory or autoimmune diseases (SIAD) and myelodysplastic syndromes (MD). This syndrome is characterized by the presence of vacuoles, X-linked inheritance, autoinflammation, and somatic mutation patterns, highlighting a unique intersection between genetic and immunological dysregulation. Apart from VEXAS, 10% to 30% of individuals diagnosed with MDS exhibit SIAD phenotypes, a significant increase compared to the 5% incidence in the general population. In this comprehensive review, we aim to elucidate the molecular mechanisms driving the pro-inflammatory environment in MDS, focusing on the contribution of VEXAS syndrome to this complex interplay. We examine how UBA1 mutations disrupt cellular homeostasis, triggering inflammatory pathways. Furthermore, we explore the broader implications of these findings for the pathogenesis of MDS, proposing that the inflammatory dysregulation of VEXAS may shed light on mechanisms of disease progression and identify potential therapeutic targets in MDS. Through an integrated analysis of genetic, immunological, and clinical data, this review seeks to deepen our understanding of the complex relationship between systemic inflammation and hematological malignancies, paving the way for new diagnostic and therapeutic strategies.

摘要

VEXAS 综合征是一种由 UBA1 基因突变引起的单基因 X 连锁疾病,它已成为揭示系统性炎症或自身免疫性疾病(SIAD)与骨髓增生异常综合征(MD)之间联系的关键模型。该综合征的特征是存在空泡、X 连锁遗传、自身炎症和体细胞突变模式,突出了遗传和免疫失调之间的独特交集。除了 VEXAS 之外,10%至 30%的 MDS 患者表现出 SIAD 表型,这一比例明显高于普通人群 5%的发病率。在这篇全面的综述中,我们旨在阐明 MDS 中促炎环境的分子机制,重点关注 VEXAS 综合征对这种复杂相互作用的贡献。我们研究了 UBA1 突变如何破坏细胞内稳态,引发炎症途径。此外,我们还探讨了这些发现对 MDS 发病机制的更广泛影响,提出 VEXAS 的炎症失调可能揭示疾病进展的机制,并确定 MDS 中的潜在治疗靶点。通过对遗传、免疫和临床数据的综合分析,本综述旨在加深我们对系统性炎症与血液恶性肿瘤之间复杂关系的理解,为新的诊断和治疗策略铺平道路。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/278a/11593025/e8b3c845a2d1/cells-13-01890-g001.jpg

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