C3G promotes bone marrow adipocyte expansion and hematopoietic regeneration after myeloablation by enhancing megakaryocyte niche function.
Herranz Ó., Berrocal P., Sicilia-Navarro C., Fernández-Infante C., Hernández-Cano L., Porras A.
Animal Study, published in J Hematol Oncol (2025) — summary generated from the PubMed abstract.
Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.
- Level A · Stronger Clinical Evidence
- Level B · Emerging clinical evidence with positive signals
- Level C · Early human research exploring benefits
- Level D · Scientific groundwork from lab and animal studies
- Emerging · Emerging topic under active research
This page is generated from the PubMed record. The Thai description is an automated summary of bibliographic fields and the abstract, not a full translation, and is not medical advice.
- Study type
- Animal Study
- Journal
- J Hematol Oncol (2025)
- Country
- England
- Reported sample size
- —
- Source database
- PubMed
- PMID
- 40170099
- DOI
- 10.1186/s13045-025-01687-1
Abstract (original English)
C3G, a Rap1 GEF, promotes megakaryopoiesis and platelet function. Using transgenic and knock-out mouse models targeting C3G in megakaryocytes, we investigated whether C3G also affects the niche function of megakaryocytes during bone marrow (BM) recovery after myeloablation induced by 5-fluorouracil (5-FU), or total body irradiation (TBI) followed by bone marrow transplantation. C3G promoted megakaryocyte maturation and platelet production during recovery, along with increased white and red blood cell counts and enhanced survival of female mice after repeated doses of 5-FU. Additionally, megakaryocytes favored adipocyte differentiation through a C3G-mediated mechanism, likely involving Fgf1. Changes in the number or behavior of BM megakaryocytes and adipocytes influenced the hematopoietic stem cell pool, with C3G promoting its bias towards the myeloid-megakaryocytic lineage in both 5-FU- and TBI-ablated models. Therefore, C3G could be a potential target in therapies aimed at enhancing hematopoiesis in patients undergoing chemotherapy and/or BM transplantation.
What this study does not prove
- • This study does not prove SVF is an approved treatment or a replacement for standard care.
- • This is preclinical work; animal or laboratory results cannot be applied to humans.
Evidence level
Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.
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