ArticleNature communications2024
Bone Marrow Endothelial Progenitor Cells remodelling facilitates normal hematopoiesis during Acute Myeloid Leukemia Complete Remission.
Article in Nature communications, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed.
- Exosomal PKM2 from AML cells reprograms endothelial metabolism to promote angiogenesis and chemoresistance.Functional & integrative genomics · 2026Article
- Bone marrow mesenchymal stem cells are functionally remodeled after complete remission of acute myeloid leukemia.Journal of translational internal medicine · 2026Article
- Immune reset: what do we learn from bone marrow transplantation.Medical review (2021) · 2026Review
- Review
- Hematopoiesis could be improved by correcting aberrant bone marrow macrophages polarization in aplastic anemia patients.Science China. Life sciences · 2026Article
- Hijacking the helpers: platelet and neutrophil trafficking in AML and therapeutic exploitation.Experimental hematology & oncology · 2026Review
- Leukemia epidemiology in China: Burden, trends, and determinants in the 21st century.Chinese journal of cancer research = Chung-kuo yen cheng yen chiu · 2025Article
- IGSF9-targeted therapy inhibits the progression of acute myeloid leukemia.Blood advances · 2025Article
- Human placenta-derived endothelial progenitor cells: an animal-free culture system for efficient expansion.Biological research · 2025Article
- HSPG2 could promote normal haematopoiesis in acute myeloid leukaemia patients after complete remission by repairing bone marrow endothelial progenitor cells.Clinical and translational medicine · 2025Article
Corrections and comments
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Authors and funding
15 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Although acute myeloid leukemia (AML) affects hematopoietic stem cell (HSC)-supportive microenvironment, it is largely unknown whether leukemia-modified bone marrow (BM) microenvironment can be remodeled to support normal hematopoiesis after complete remission (CR). As a key element of BM microenvironment, endothelial progenitor cells (EPCs) provide a feasible way to investigate BM microenvironment remodeling. Here, we find reduced and dysfunctional BM EPCs in AML patients, characterized by impaired angiogenesis and high ROS levels, could be partially remodeled after CR and improved by N-acetyl-L-cysteine (NAC). Importantly, HSC-supporting ability of BM EPCs is partially recovered, whereas leukemia-supporting ability is decreased in CR patients. Mechanistically, the transcriptome characteristics of leukemia-modified BM EPCs return to near-normal after CR. In a classic AML mouse and chemotherapy model, BM vasculature and normal hematopoiesis are reversed after CR. In summary, we provide further insights into how leukemia-modified BM microenvironment can be remodeled to support normal hematopoiesis after CR, which can be further improved by NAC.
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