Evidence map›Paper›PMID 37721853›Full record

ArticleThe Journal of clinical investigation2023

GLUT3 promotes macrophage signaling and function via RAS-mediated endocytosis in atopic dermatitis and wound healing.

Dong-Min Yu, Jiawei Zhao, Eunice E Lee, Dohun Kim, Ruchika Mahapatra, Elysha K Rose, Zhiwei Zhou, Calvin Hosler, Abdullah El Kurdi, Jun-Yong Choe and 6 more

Open access · goldAbstract read
In one paragraph

Article in The Journal of clinical investigation, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.

0numbers the graph read from it
0cells of the map it votes in
34citing papers in PubMed
12.0field-weighted citation impact, top 1% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

34 citing papers in PubMed, 42 citations in OpenAlex.

  1. Article
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  8. Insulin Resistance and Inflammation.International journal of molecular sciences · 2026
    Review
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  13. Article
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  15. Regulation of macrophage transcriptional dynamics during acute and chronic wound repair.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2025
    Review
  16. Article
  17. Article
  18. IGF2BP3-mediated mBone research · 2025
    Article
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

16 authors at 7 institutions in 3 countries.

Dong-Min YuDepartment of Dermatology, UT Southwestern Medical Center, Dallas, Texas, USA.
Jiawei ZhaoDivision of Hematology/Oncology, Boston Children's Hospital and Department of Pediatric Oncology, Dana-Farber Cancer Institute, Harvard Medical School, Boston, Massachusetts, USA.
Eunice E LeeDepartment of Dermatology, UT Southwestern Medical Center, Dallas, Texas, USA.
Dohun KimChildren's Medical Center Research Institute and.
Ruchika MahapatraDepartment of Dermatology, UT Southwestern Medical Center, Dallas, Texas, USA.
Elysha K RoseDepartment of Dermatology, UT Southwestern Medical Center, Dallas, Texas, USA.
Zhiwei ZhouDepartments of Biochemistry and Radiation Oncology, UT Southwestern Medical Center, Dallas, Texas, USA.
Calvin HoslerDepartment of Dermatology, UT Southwestern Medical Center, Dallas, Texas, USA.
Abdullah El KurdiDepartment of Biochemistry and Molecular Genetics, American University of Beirut, Beirut, Lebanon.
Jun-Yong ChoeDepartment of Chemistry and Chemical Biology, University of New Mexico, Albuquerque, New Mexico, USA.
E Dale AbelDepartment of Medicine, David Geffen School of Medicine, UCLA, Los Angeles, California, USA.
Gerta HoxhajChildren's Medical Center Research Institute and.
Kenneth D WestoverDepartments of Biochemistry and Radiation Oncology, UT Southwestern Medical Center, Dallas, Texas, USA.
Raymond J ChoDepartment of Dermatology, UCSF, San Francisco, California, USA.
Jeffrey B ChengDepartment of Dermatology, UCSF, San Francisco, California, USA.
Richard C WangDepartment of Dermatology, UT Southwestern Medical Center, Dallas, Texas, USA.
Southwestern Medical Center · USChildren's Medical Center · USUniversity of California, San Francisco · USAmerican University of Beirut · LBBroad Institute · USUniversity of California, Los Angeles · USUniversity of New Mexico · US

Funding

UT Southwestern Medical Center Simmons Comprehensive Cancer CenterP30CA142543 · NCI · UT SOUTHWESTERN MEDICAL CENTER · PI MELANIE H. COBB · 2010 to 2026
$53.7M
UT Southwestern NORCP30DK127984 · NIDDK · UT SOUTHWESTERN MEDICAL CENTER · PI Jeff G McDonald · 2022 to 2026
$7.4M
Characterization and targeting of rapid nucleotide exchange RAS mutationsR01CA244341 · NCI · UT SOUTHWESTERN MEDICAL CENTER · PI WESTOVER, KENNETH · 2020 to 2024
$1.8M
Mechanisms of Glucose Dependence in Proliferating CellsR01AR072655 · NIAMS · UT SOUTHWESTERN MEDICAL CENTER · PI WANG, RICHARD C · 2018 to 2022
$1.7M
NCI NIH HHS P30 CA142543NCI NIH HHS R01 CA244341NIAMS NIH HHS R01 AR072655NIDDK NIH HHS P30 DK127984
6 · The paper itself

Abstract

The facilitative GLUT1 and GLUT3 hexose transporters are expressed abundantly in macrophages, but whether they have distinct functions remains unclear. We confirmed that GLUT1 expression increased after M1 polarization stimuli and found that GLUT3 expression increased after M2 stimulation in macrophages. Conditional deletion of Glut3 (LysM-Cre Glut3fl/fl) impaired M2 polarization of bone marrow-derived macrophages. Alternatively activated macrophages from the skin of patients with atopic dermatitis showed increased GLUT3 expression, and a calcipotriol-induced model of atopic dermatitis was rescued in LysM-Cre Glut3fl/fl mice. M2-like macrophages expressed GLUT3 in human wound tissues as assessed by transcriptomics and costaining, and GLUT3 expression was significantly decreased in nonhealing, compared with healing, diabetic foot ulcers. In an excisional wound healing model, LysM-Cre Glut3fl/fl mice showed significantly impaired M2 macrophage polarization and delayed wound healing. GLUT3 promoted IL-4/STAT6 signaling, independently of its glucose transport activity. Unlike plasma membrane-localized GLUT1, GLUT3 was localized primarily to endosomes and was required for the efficient endocytosis of IL-4Rα subunits. GLUT3 interacted directly with GTP-bound RAS in vitro and in vivo through its intracytoplasmic loop domain, and this interaction was required for efficient STAT6 activation and M2 polarization. PAK activation and macropinocytosis were also impaired without GLUT3, suggesting broader roles for GLUT3 in the regulation of endocytosis. Thus, GLUT3 is required for efficient alternative macrophage polarization and function, through a glucose transport-independent, RAS-mediated role in the regulation of endocytosis and IL-4/STAT6 activation.

Indexed as

Dermatitis, AtopicAnimalsEndocytosisGlucoseGlucose Transporter Type 1Glucose Transporter Type 3HumansInterleukin-4Macrophage ActivationMacrophagesMiceWound HealingGlucoseGlucose Transporter Type 1Glucose Transporter Type 3Interleukin-4SLC2A3 protein, humanSlc2a3 protein, mouseDermatologyGlucose metabolismImmunologyMacrophagesSkin

Identifiers

PMID37721853
PMCPMC10617774
OpenAlexW4386826490

What OpenQuestion holds

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Registered trials

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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 OpenQuestion graph.