ArticleCells2026
Glutamine Depletion Induced Senescence-Associated β-Galactosidase Activity and Impaired Functional Properties of Ea.hy926 Endothelial Cells.
Article in Cells, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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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.
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Authors and funding
4 authors.
Funding
Abstract
Glutamine is a conditionally essential amino acid that is important for endothelial homeostasis, while endothelial cell dysfunction is associated with altered glutamine metabolism and shifts toward stress-responsive pathways. We investigated the role of glutamine and senescence-associated beta-galactosidase (SA-β-gal) activity in Ea.hy926 endothelial cells (ECs), together with supportive functional activity assays. We found that glutamine depletion induced a progressive decline in endothelial function. Specifically, glutamine-depleted ECs exhibited increased SA-β-gal activity, accompanied by impaired proliferative capacity, disrupted cellular morphogenesis, increased promyelocytic cell adhesion, and diminished ability to promote host tissue proliferation and EC morphogenesis in a zebrafish xenograft model. These findings suggest that glutamine availability is crucial for maintaining endothelial integrity and functional competence.
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