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Within the hematopoietic system, EVs orchestrate critical signaling between bone marrow (BM) niche cells and hematopoietic stem and progenitor cells (HSPCs) to regulate quiescence, proliferation, and lineage commitment. During aging, senescence and telomere attrition drive a profound remodeling of EV biogenesis and cargo. Aged EVs, particularly those released from senescent mesenchymal stromal cells (MSCs) and osteoblasts, exhibit altered microRNA profiles and reduced protective antioxidants. These changes perpetuate niche dysfunction, induce senescence in recipient cells, and promote myeloid\u2010biased hematopoiesis. Importantly, this communication is a selective process governed by vesicle\u2010intrinsic surface signatures, such as tetraspanins and integrins, which interact with specific receptors on distinct hematopoietic subsets to regulate signaling fidelity. Conversely, EVs from young or pluripotent stem cells deliver rejuvenating signals that can restore aged HSPC function and attenuate inflammaging. Elucidating these mechanisms of selective targeting and stress\u2010responsive cargo remodeling provides vital insights for developing EV\u2010based diagnostic tools and rejuvenation strategies to prevent age\u2010related immune imbalances and hematologic malignancies.<\/jats:p>","DOI":"10.1111\/acel.70715","type":"journal-article","created":{"date-parts":[[2026,9,24]],"date-time":"2026-09-24T04:50:12Z","timestamp":1790225412000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":0,"title":["The Role of\n                    <scp>EVs<\/scp>\n                    in the Aging Hematopoietic System"],"prefix":"10.1111","volume":"25","author":[{"ORCID":"https:\/\/orcid.org\/0009-0002-4378-9729","authenticated-orcid":false,"given":"Esra G.","family":"Kosebent","sequence":"first","affiliation":[{"name":"School of Cancer Sciences, University of Glasgow  Glasgow 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