ArticleiScience2026
Plasma membrane mediated GLUT10 mitochondrial targeting regulates intracellular ascorbic acid homeostasis.
Article in iScience, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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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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Who cites it
1 citing paper in PubMed.
- Glucose Transporters: Structure, Trafficking, Physiology, and Disease Relevance.Current issues in molecular biology · 2026Review
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Authors and funding
11 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Intracellular ascorbic acid (AA) regulation is essential for connective tissue homeostasis; however, the precise mechanisms governing AA homeostasis during cellular stress remain poorly understood. Here, we identify an oxidative stress-induced glucose transporter 10 (GLUT10) intracellular trafficking mechanism that regulates AA homeostasis via a noncanonical route from the endoplasmic reticulum (ER) to the plasma membrane (PM) and ultimately to mitochondria. This mechanism bridges the traditionally considered spatially and mechanistically distinct pathways of endomembrane system trafficking and mitochondria targeting. Using live-cell imaging and complementary biochemical approaches, we demonstrate that oxidative stress drives this redistribution. Increased PM localization of GLUT10 enhances the uptake of dehydroascorbic acid (DHA), the oxidized form of AA, thereby sustaining intracellular AA levels. The disruption of this trafficking pathway impairs AA homeostasis. Our findings reveal previously unrecognized localization of GLUT10 at the PM and endosomes and uncover endomembrane-mitochondria communication that maintains intracellular AA homeostasis and supports adaptation to oxidative stress.
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