ArticleExtracellular vesicle2026
Extracellular vesicle cargo dynamics in the bone marrow microenvironment: from hematopoietic homeostasis to malignant transformation.
Article in Extracellular vesicle, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors.
Funding
Abstract
The bone marrow (BM) microenvironment relies on extracellular vesicle (EV)-mediated communication to maintain hematopoietic homeostasis and contribute to cellular responses in malignant transformation. EV function as molecular shuttles carrying miRNAs, proteins, and lipids that regulate hematopoietic stem cell (HSC) self-renewal, quiescence, and lineage commitment. HSC-derived EVs can stimulate stem cell factor (SCF) expression in recipient HSCs through autocrine/paracrine signaling, while mesenchymal stem cell (MSC)-EVs modulate HSC differentiation via TLR4 activation and miRNA transfer. Regulated EV biogenesis pathways, involving tetraspanins, ESCRT components, and lipid-sorting mechanisms, control cargo selection and secretion in both HSCs and BM cells. During malignant transformation, EV cargo composition shifts dramatically: leukemic cells release EVs enriched in immunosuppressive factors, pro-survival signals, and drug resistance mediators that reprogram the BM microenvironment to support tumor growth. These changes-driven by hypoxia, inflammatory signaling, metabolic reprogramming, and chemotherapeutic pressure-enable tumor-derived EVs to induce HSC quiescence, polarize macrophages toward immunosuppressive phenotypes, and promote stromal cell transformation. The distinct protein and miRNA profiles of EVs from malignant versus healthy cells offer diagnostic and prognostic value, positioning EVs as both biomarkers and therapeutic targets. This review examines EV cargo composition and functional roles in normal and malignant hematopoiesis, emphasizing dynamic changes that accompany disease progression and their clinical implications.
Indexed as
Identifiers
What Socratic holds
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 Socratic graph.