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<p>Aplastic anemia (AA) is a life-threatening bone marrow (BM) failure syndrome characterized by pancytopenia. Recent studies revealed that dysfunctional endothelial progenitor cells (EPCs), critical components of the BM microenvironment, are involved in hematopoietic-dysfunction-related diseases, including AA. However, the mechanism underlying EPC damage in AA remains unknown. Here we find that transforming growth factor-β (TGF-β) signaling is hyperactive in dysfunctional AA EPCs with impaired hematopoietic support and immune regulatory ability, and TGF-β inhibition promotes hematopoiesis and immune rebalance by repairing dysfunctional EPCs. Through impaired EPC and AA murine models, we validated that TGF-β inhibition restores EPC dysfunction to improve hematopoiesis and immune status in vitro and in vivo. RNA sequencing and real-time quantitative polymerase chain reaction provided further validation. These results indicate that dysfunctional BM EPCs with hyperactive TGF-β signaling are involved in AA. TGF-β inhibition promotes multilineage hematopoiesis recovery and immune balance by repairing dysfunctional EPCs, providing a potential therapeutic strategy for AA.</p><p></p>

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TGF-β inhibition restores hematopoiesis and immune balance via bone marrow EPCs in aplastic anemia

  • 期刊论文

  • 出版模式：

    开放获取

  • 发表日期：

    2025年6月30日

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  • Xin-Yan Zhang,
  • Li-Ping Guo,
  • Ya-Zhe Wang,
  • Jin-Song Jia,
  • Mi Liang,
  • Meng-Zhu Shen,
  • Zhen-Kun Wang,
  • Zhi-Wei Zhang,
  • Chen-Yuan Li,
  • Zhong-Shi Lyu,
  • Tong Xing,
  • Yuan-Yuan Zhang,
  • Xiao-Jun Huang,
  • Yuan Kong

摘要

Aplastic anemia (AA) is a life-threatening bone marrow (BM) failure syndrome characterized by pancytopenia. Recent studies revealed that dysfunctional endothelial progenitor cells (EPCs), critical components of the BM microenvironment, are involved in hematopoietic-dysfunction-related diseases, including AA. However, the mechanism underlying EPC damage in AA remains unknown. Here we find that transforming growth factor-β (TGF-β) signaling is hyperactive in dysfunctional AA EPCs with impaired hematopoietic support and immune regulatory ability, and TGF-β inhibition promotes hematopoiesis and immune rebalance by repairing dysfunctional EPCs. Through impaired EPC and AA murine models, we validated that TGF-β inhibition restores EPC dysfunction to improve hematopoiesis and immune status in vitro and in vivo. RNA sequencing and real-time quantitative polymerase chain reaction provided further validation. These results indicate that dysfunctional BM EPCs with hyperactive TGF-β signaling are involved in AA. TGF-β inhibition promotes multilineage hematopoiesis recovery and immune balance by repairing dysfunctional EPCs, providing a potential therapeutic strategy for AA.