ArticleStem cells (Dayton, Ohio)2026
Age-associated T cell immunity decreases circulating endothelial progenitor cells.
Article in Stem cells (Dayton, Ohio), 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
What it found
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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
1 citing paper in PubMed.
- Mitochondria-Associated mRNAs Restore ATP During Oxidative Stress via Cytosolic Translation.Antioxidants (Basel, Switzerland) · 2026Article
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PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
13 authors.
Funding
Abstract
A reduction in circulating endothelial progenitor cells (EPCs) comprise an important part of vascular aging. However, the underlying mechanisms that mediate this EPC decline remain unclear. Here, we demonstrate a novel molecular mechanism where aging increases inhibitory T cell subsets and impairs SDF1-mediated increase of circulating EPCs. SomaScan proteomics and western blot analysis revealed FABP4 as the top upregulated protein in plasma and was also increased in the bone marrow in aging. Importantly, treatment with FABP4 in bone marrow cells increased inhibitory T cells while decreased SDF-1 receptor, CXCR4 in EPCs, whereas blocking FABP4 signaling by BMS309403 or depleting these T cells restored surface expression of CXCR4 in EPCs. Notably, FABP4-mediated decrease of circulating EPC in aging were restored by therapeutic administration of mitochondria, wherein plasma FABP4 was decreased along with reducing inhibitory T cell induction in bone marrow and increasing circulating EPCs in older mice. Collectively, these findings provide new insight into the involvement of age-associated T cell immunity in EPC dysregulation, and FABP4 may be a therapeutic target to detain vascular aging.
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