ArticleNature communications2025
Inflammatory stromal and T cells mediate human bone marrow niche remodeling in clonal hematopoiesis and myelodysplasia.
Article in Nature communications, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers, 1 of them a synthesis that pooled it.
What it found
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
20 citing papers in PubMed, 1 synthesis or guideline pooled it.
- The proteomic architecture of clonal hematopoiesis: a systematic review of niche remodeling and multi-compartment predictors of malignant transformation.Frontiers in medicine · 2026Pooled it
- Bone health in myelodysplastic neoplasms: results from the prospective longitudinal BoHemE study.Leukemia · 2026Article
- Mechanisms of Hematopoietic Stem Cell Aging and Emerging Rejuvenation Strategies.Stem cell reviews and reports · 2026Review
- Prefibrotic bone marrow microenvironment is a hallmark of clonal hematopoiesis.Nature immunology · 2026Article
- Clonal blood reshapes its home.Nature immunology · 2026Article
- Spatially resolved transcriptomic profiling of myelofibrosis spleen reveals compartment specific niche programs.Experimental hematology & oncology · 2026Article
- Stromal cell senescence augments haematopoietic cell fitness in clonal haematopoiesis.Nature cell biology · 2026Article
- Clonal hematopoiesis of indeterminate potential (CHIP)-a pivotal contributor of aging and related disorders.Annals of translational medicine · 2026Review
- Inflammatory Signatures in MDS: The Missing Link Between Genetics, Microenvironment, and Therapy.Cells · 2026Review
- Immunosenescence in systemic and multi-organ aging: mechanisms, inter-organ crosstalk, and translational opportunities.npj aging · 2026Review
- Review
- Molecular frontiers of fungal autophagy: from molecular mechanisms to potential targets for antifungal drug discovery.World journal of microbiology & biotechnology · 2026Review
- Construction Strategies and Advances in Bone Marrow Microphysiological Systems.International journal of molecular sciences · 2026Review
- Nestin/CXCL12 immunohistochemistry and RNA sequencing map the bone marrow microenvironment in aplastic anemia.Disease models & mechanisms · 2026Article
- Preclinical efficacy of tasquinimod in myelodysplastic neoplasms: Restoring erythropoiesis and mitigating bone loss.HemaSphere · 2026Article
- Decoding the tumor-aging axis: from bench to clinical.Frontiers in immunology · 2026Review
- Causal association between clonal hematopoiesis indeterminate potential and cancer: a Mendelian randomization study.Experimental biology and medicine (Maywood, N.J.) · 2026Article
- Pediatric leukemia: origins, pathogenesis, the role of microenvironment and immunological modulation.Frontiers in immunology · 2026Review
- T lymphocytes and natural killer cells in myelodysplastic syndromes: function, dysfunction, and therapeutic potential.Frontiers in immunology · 2026Review
- An inflammatory T-cell-stromal axis contributes to hematopoietic stem/progenitor cell failure and clonal evolution in human myelodysplastic syndrome.Nature communications · 2025Article
Corrections and comments
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Authors and funding
24 authors.
Funding
Abstract
Somatic mutations in hematopoietic stem/progenitor cells (HSPCs) can lead to clonal hematopoiesis of indeterminate potential (CHIP) and progression to myelodysplastic syndromes (MDS). Using single-cell and anatomical profiling of a large cohort of human bone marrow (BM), we show that the HSPC BM niche in CHIP and MDS is undergoing inflammatory remodeling. This includes loss of CXCL12⁺ adipogenic stromal cells and the emergence of a distinct population of inflammatory mesenchymal stromal cells (iMSCs), which arise in CHIP and become more prevalent in MDS. Functional studies in primary BM HSPC-MSC co-cultures reveals that healthy aged and CHIP HSPCs activate stromal support, while MDS HSPCs fail to do so. In contrast, MDS blasts further suppress HSPC support and trigger inflammation, indicating disease-stage-specific stromal disruption. In parallel, we show that iMSCs retain partial support and angiogenic potential in MDS, coinciding with expanded BM vasculature. Additionally, we identify IFN-responsive T cells that preferentially interact with iMSCs, potentially reinforcing local inflammation. These findings position iMSCs as central mediators of early BM niche dysfunction and potential therapeutic targets for intercepting pre-malignant hematopoiesis.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.