Evidence map›Paper›PMID 32428862›Full record

ArticleiScience2020

Solute Carrier Family 37 Member 2 (SLC37A2) Negatively Regulates Murine Macrophage Inflammation by Controlling Glycolysis.

Zhan Wang, Qingxia Zhao, Yan Nie, Yi Yu, Biswapriya B Misra, Manal Zabalawi, Jeff W Chou, Chia-Chi C Key, Anthony J Molina, Matthew A Quinn and 4 more

Open access · goldAbstract read
In one paragraph

Article in iScience, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
1.3field-weighted citation impact, top 20% 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

13 citing papers in PubMed, 31 citations in OpenAlex.

  1. Structural basis of glucose-6-phosphate transport by human SLC37A2.Nature structural & molecular biology · 2026
    Article
  2. Piceatannol Attenuates Benzo[Journal of agricultural and food chemistry · 2025
    Article
  3. Article
  4. The role of mFrontiers in immunology · 2025
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

14 authors at 3 institutions in 2 countries.

Zhan WangDepartment of Internal Medicine, Section of Molecular Medicine, Wake Forest School of Medicine, Winston-Salem, NC 27157, USA.
Qingxia ZhaoDepartment of Internal Medicine, Section of Molecular Medicine, Wake Forest School of Medicine, Winston-Salem, NC 27157, USA.
Yan NieDepartment of Internal Medicine, Section of Molecular Medicine, Wake Forest School of Medicine, Winston-Salem, NC 27157, USA.
Yi YuDepartment of Internal Medicine, Section of Molecular Medicine, Wake Forest School of Medicine, Winston-Salem, NC 27157, USA; Department of Pediatrics, Ruijin Hospital, Shanghai Jiaotong University School of Medicine, Shanghai 200025, China.
Biswapriya B MisraDepartment of Internal Medicine, Section of Molecular Medicine, Wake Forest School of Medicine, Winston-Salem, NC 27157, USA.
Manal ZabalawiDepartment of Internal Medicine, Section of Molecular Medicine, Wake Forest School of Medicine, Winston-Salem, NC 27157, USA.
Jeff W ChouDivision of Public Health Sciences, Wake Forest School of Medicine, Winston-Salem, NC 27157, USA.
Chia-Chi C KeyDepartment of Internal Medicine, Section of Molecular Medicine, Wake Forest School of Medicine, Winston-Salem, NC 27157, USA.
Anthony J MolinaDepartment of Internal Medicine, Section on Gerontology and Geriatric Medicine, Wake Forest School of Medicine, Winston-Salem, NC 27157, USA.
Matthew A QuinnDepartment of Pathology, Wake Forest School of Medicine, Winston-Salem, NC 27157, USA.
Michael B FesslerImmunity, Inflammation and Disease Laboratory, National Institute of Environmental Health Sciences, NIH, Research Triangle Park, NC 27709, USA.
John S ParksDepartment of Internal Medicine, Section of Molecular Medicine, Wake Forest School of Medicine, Winston-Salem, NC 27157, USA.
Charles E McCallDepartment of Internal Medicine, Section of Molecular Medicine, Wake Forest School of Medicine, Winston-Salem, NC 27157, USA; Department of Microbiology and Immunology, Wake Forest School of Medicine, Winston-Salem, NC 27157, USA.
Xuewei ZhuDepartment of Internal Medicine, Section of Molecular Medicine, Wake Forest School of Medicine, Winston-Salem, NC 27157, USA; Department of Microbiology and Immunology, Wake Forest School of Medicine, Winston-Salem, NC 27157, USA. Electronic address: xwzhu@wakehealth.edu.
Wake Forest University · USNational Institute of Environmental Health Sciences · USRuijin Hospital · CN

Funding

Tumor Tissue CoreP30CA012197 · NCI · WAKE FOREST UNIVERSITY HEALTH SCIENCES · PI Ruben A. Mesa · 1985 to 2026
$55.4M
Cell Signaling of Host DefenseZIAES102005 · NIEHS · NATIONAL INSTITUTE OF ENVIRONMENTAL HEALTH SCIENCES · PI FESSLER, MICHAEL B · 2009 to 2025
$41.7M
The Role of Hepatocyte ABCA1 in Lipid Mobilization and TransportR01HL119962 · NHLBI · WAKE FOREST UNIVERSITY HEALTH SCIENCES · PI PARKS, JOHN S · 2013 to 2022
$3.9M
Cell Signaling of Host DefenseZ01ES102005 · NIEHS · NATIONAL INSTITUTE OF ENVIRONMENTAL HEALTH SCIENCES · PI FESSLER, MICHAEL B · 2006 to 2008
$3.3M
Redox control over metabolism and mitochondrial bioenergetics directs the course of acute inflammation and sepsisR35GM126922 · NIGMS · WAKE FOREST UNIVERSITY HEALTH SCIENCES · PI MCCALL, CHARLES EMORY · 2018 to 2022
$2.1M
The role of SLC37A2, a glucose 6 phosphate transporter, in inflammation and metabolic diseasesR01HL132035 · NHLBI · WAKE FOREST UNIVERSITY HEALTH SCIENCES · PI ZHU, XUEWEI · 2016 to 2020
$1.9M
Intramural NIH HHS Z01 ES102005NCI NIH HHS P30 CA012197NHLBI NIH HHS R01 HL119962NHLBI NIH HHS R01 HL132035NIGMS NIH HHS R35 GM126922
6 · The paper itself

Abstract

Increased flux of glucose through glycolysis is a hallmark of inflammatory macrophages and is essential for optimal effector functions. Solute carrier (SLC) 37A2 is an endoplasmic reticulum-anchored phosphate-linked glucose-6-phosphate transporter that is highly expressed in macrophages and neutrophils. We demonstrate that SLC37A2 plays a pivotal role in murine macrophage inflammatory activation and cellular metabolic rewiring. Toll-like receptor (TLR) 4 stimulation by lipopolysaccharide (LPS) rapidly increases macrophage SLC37A2 protein expression. SLC37A2 deletion reprograms macrophages to a hyper-glycolytic process and accelerates LPS-induced inflammatory cytokine production, which partially depends on nicotinamide adenine dinucleotide (NAD

Indexed as

Cell BiologyFunctional Aspects of Cell BiologyImmunologyMetabolism

Identifiers

PMID32428862
PMCPMC7232099
OpenAlexW3022877454

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

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.