Munteanu Raluca, Gulei Diana, Moldovan Cristian Silviu, Azzoni Emanuele, Belver Laura, Feder Richard, Pirv Simina, Buzoianu Anca Dana, Einsele Hermann, Mittelman Moshe, Ghiaur Gabriel, Hasserjian Robert, Tomuleasa Ciprian
Department of Personalized Medicine and Rare Diseases, Medfuture Institute for Biomedical Research, Iuliu Hațieganu University of Medicine and Pharmacy, Cluj-Napoca, Romania.
Department of Nanosciences, Medfuture Institute for Biomedical Research, Iuliu Hațieganu University of Medicine and Pharmacy, Cluj-Napoca, Romania.
Cell Death Dis. 2025 Jul 17;16(1):531. doi: 10.1038/s41419-025-07861-0.
Myelodysplastic syndromes (MDS) are heterogeneous hematopoietic stem cell disorders defined by ineffective hematopoiesis, multilineage dysplasia, and risk of progression to acute myeloid leukemia. Improvements have been made to identify recurrent genetic mutations and their functional roles, but translating this into preclinical models is still difficult. Traditional murine systems lack the human-specific cytokine support and microenvironmental support that is necessary to reproduce MDS pathophysiology. Humanized mouse models, particularly those incorporating human cytokines (e.g., MISTRG, NSG-SGM3, NOG-EXL), immunodeficient backgrounds, and co-transplantation strategies, have improved the engraftment and differentiation of human hematopoietic stem and progenitor cells. These models allow the study of clonal evolution, mutation-specific disease dynamics, and response to therapies in vivo. However, difficulties persist, such as limited long-term engraftment, incomplete immune reconstruction, and limited possibilities of modeling early-stage or low-risk MDS. This review presents an overview of current humanized and genetically engineered mouse models suitable for studying MDS, evaluating their capacity to replicate disease complexity, preserve clonal architecture, and support translational research. We highlight the need to develop new approaches to improve the actual methodologies and propose future directions for standardization and improved clinical relevance.
骨髓增生异常综合征(MDS)是一类异质性造血干细胞疾病,其特征为造血无效、多系发育异常以及进展为急性髓系白血病的风险。在识别复发性基因突变及其功能作用方面已取得进展,但将其转化为临床前模型仍很困难。传统的小鼠系统缺乏重现MDS病理生理学所需的人类特异性细胞因子支持和微环境支持。人源化小鼠模型,特别是那些整合了人类细胞因子(如MISTRG、NSG-SGM3、NOG-EXL)、免疫缺陷背景和共移植策略的模型,已改善了人类造血干细胞和祖细胞的植入和分化。这些模型允许在体内研究克隆进化、突变特异性疾病动态以及对治疗的反应。然而,困难依然存在,如长期植入有限、免疫重建不完全以及模拟早期或低风险MDS的可能性有限。本综述概述了目前适用于研究MDS的人源化和基因工程小鼠模型,评估它们复制疾病复杂性、保留克隆结构以及支持转化研究的能力。我们强调需要开发新方法来改进实际方法,并提出标准化和提高临床相关性的未来方向。