ArticleEMBO molecular medicine2026
Endothelial SLC25A13 links glutamine metabolism to angiogenesis.
Article in EMBO molecular medicine, 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
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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
23 authors.
Funding
Abstract
Attention to exploring endothelial cell (EC) metabolism is increasing, but a holistic perspective on the metabolic adaptations of ECs during angiogenic proliferation is still missing. Here, we use a previously in-house developed computational EC-adapted genome-scale metabolic model that recapitulates known metabolic features in proliferating ECs to predict novel pathways central to biomass synthesis. We unveil the metabolic function of the glutamate-aspartate antiporter SLC25A13, previously overlooked in ECs, as a key regulator of glutamine utilization and provide evidence regarding its contribution to the generation of cholesterol and other biomass precursors. To our knowledge, predominant SLC25A13-linked utilization of glutamine for cholesterol synthesis has not been reported in other cell types in prior literature. Silencing of SLC25A13 in ECs reduced proliferation and vessel sprouting in vitro as well as in a choroidal neovascularization mouse model. These insights underscore the particular characteristics of EC metabolism and may warrant further evaluation of SLC25A13 as a putative new anti-angiogenic target.
Identifiers
42800829What 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.