GLUT3 regulates alternative macrophage signaling through a glucose transport–independent role

Macrophages are key mediators of innate immunity whose functional state can be regulated by glucose transporters. Although abundantly expressed in macrophages, the specific function of GLUT3, an isoform of facilitative glucose transporters, has not been clearly established. In this issue of the JCI,...

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Main Authors: Peng Zhang, Jason Miska, Amy B. Heimberger
Format: Article
Language:English
Published: American Society for Clinical Investigation 2023-11-01
Series:The Journal of Clinical Investigation
Online Access:https://doi.org/10.1172/JCI174540
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author Peng Zhang
Jason Miska
Amy B. Heimberger
author_facet Peng Zhang
Jason Miska
Amy B. Heimberger
author_sort Peng Zhang
collection DOAJ
description Macrophages are key mediators of innate immunity whose functional state can be regulated by glucose transporters. Although abundantly expressed in macrophages, the specific function of GLUT3, an isoform of facilitative glucose transporters, has not been clearly established. In this issue of the JCI, Dong-Min Yu and colleagues identify an alternative role for GLUT3 in promoting M2 macrophage polarization. The authors demonstrated that GLUT3 was upregulated upon M2 stimulation and was required for efficient alternative macrophage polarization and function. They further showed that GLUT3-induced M2 polarization was independent of glucose transport and functioned through Ras-mediated regulation of IL-4R endocytosis and IL-4/STAT6 activation. These findings may guide the development of macrophage-targeted treatments.
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spelling doaj.art-6da00be9823a40a38420a43706d970ef2023-11-07T16:21:03ZengAmerican Society for Clinical InvestigationThe Journal of Clinical Investigation1558-82382023-11-0113321GLUT3 regulates alternative macrophage signaling through a glucose transport–independent rolePeng ZhangJason MiskaAmy B. HeimbergerMacrophages are key mediators of innate immunity whose functional state can be regulated by glucose transporters. Although abundantly expressed in macrophages, the specific function of GLUT3, an isoform of facilitative glucose transporters, has not been clearly established. In this issue of the JCI, Dong-Min Yu and colleagues identify an alternative role for GLUT3 in promoting M2 macrophage polarization. The authors demonstrated that GLUT3 was upregulated upon M2 stimulation and was required for efficient alternative macrophage polarization and function. They further showed that GLUT3-induced M2 polarization was independent of glucose transport and functioned through Ras-mediated regulation of IL-4R endocytosis and IL-4/STAT6 activation. These findings may guide the development of macrophage-targeted treatments.https://doi.org/10.1172/JCI174540
spellingShingle Peng Zhang
Jason Miska
Amy B. Heimberger
GLUT3 regulates alternative macrophage signaling through a glucose transport–independent role
The Journal of Clinical Investigation
title GLUT3 regulates alternative macrophage signaling through a glucose transport–independent role
title_full GLUT3 regulates alternative macrophage signaling through a glucose transport–independent role
title_fullStr GLUT3 regulates alternative macrophage signaling through a glucose transport–independent role
title_full_unstemmed GLUT3 regulates alternative macrophage signaling through a glucose transport–independent role
title_short GLUT3 regulates alternative macrophage signaling through a glucose transport–independent role
title_sort glut3 regulates alternative macrophage signaling through a glucose transport independent role
url https://doi.org/10.1172/JCI174540
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AT jasonmiska glut3regulatesalternativemacrophagesignalingthroughaglucosetransportindependentrole
AT amybheimberger glut3regulatesalternativemacrophagesignalingthroughaglucosetransportindependentrole