Bahmani Forouzan, Shayanmanesh Maryam, Safari Mahdi, Alaei Amirarsalan, Rasti Zahra, Zaker Farhad, Rostami Shahrbano, Damerchiloo Fatemeh, Safa Majid
Department of Hematology and Blood Banking, Faculty of Allied Medicine, Iran University of Medical Sciences, Tehran, Iran.
Immunology Research Center, Tabriz University of Medical Science, Tabriz, Iran.
Cancer Cell Int. 2025 May 10;25(1):175. doi: 10.1186/s12935-025-03793-z.
Myelodysplastic neoplasms (MDS) represent a heterogeneous group of malignant hematopoietic stem and progenitor cell (HSPC) disorders characterized by cytopenia, ineffective hematopoiesis, as well as the potential to progress to acute myeloid leukemia (AML). The pathogenesis of MDS is influenced by intrinsic factors, such as genetic insults, and extrinsic factors, including altered bone marrow microenvironment (BMM) composition and architecture. BMM is reprogrammed in MDS, initially to prevent the development of the disease but eventually to provide a survival advantage to dysplastic cells. Recently, inflammation or age-related inflammation in the bone marrow has been identified as a key pathogenic mechanism for MDS. Inflammatory signals trigger stress hematopoiesis, causing HSPCs to emerge from quiescence and resulting in MDS development. A better understanding of the role of the BMM in the pathogenesis of MDS has opened up new avenues for improving diagnosis, prognosis, and treatment of the disease. This article provides a comprehensive review of the current knowledge regarding the significance of the BMM to MDS pathophysiology and highlights recent advances in developing innovative therapies.
骨髓增生异常肿瘤（MDS）是一组异质性的恶性造血干细胞和祖细胞（HSPC）疾病，其特征为血细胞减少、无效造血以及进展为急性髓系白血病（AML）的可能性。MDS的发病机制受内在因素影响，如基因损伤，也受外在因素影响，包括骨髓微环境（BMM）组成和结构的改变。BMM在MDS中会发生重编程，最初是为了预防疾病发展，但最终是为发育异常的细胞提供生存优势。最近，骨髓中的炎症或与年龄相关的炎症已被确定为MDS的关键致病机制。炎症信号触发应激造血，导致HSPC从静止状态中出现并引发MDS的发展。对BMM在MDS发病机制中的作用有了更好的理解，为改善该疾病的诊断、预后及治疗开辟了新途径。本文全面综述了当前关于BMM对MDS病理生理学意义的认识，并强调了开发创新疗法的最新进展。
