Evidence map›Paper›PMID 38197509›Full record

ArticleJournal of leukocyte biology2024

TGFβ macrophage reprogramming: a new dimension of macrophage plasticity.

Mary A Oliver, Xenia D Davis, Julia K Bohannon

Open access · greenAbstract read
In one paragraph

Article in Journal of leukocyte biology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
3.8field-weighted citation impact, top 6% 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

19 citing papers in PubMed, 16 citations in OpenAlex.

  1. Type I interferon-induced CD169Journal of periodontology · 2026
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  13. NuclearJournal of clinical & cellular immunology · 2025
    Article
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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

3 authors at 1 institution in 1 country.

Mary A OliverDepartment of Pathology, Microbiology and Immunology, Vanderbilt University Medical Center, 1161 21st Avenue South, Nashville, TN, 37232.
Xenia D DavisDepartment of Anesthesiology, Vanderbilt University Medical Center, 1161 21st Avenue South, Nashville, TN, 37232.
Julia K BohannonDepartment of Pathology, Microbiology and Immunology, Vanderbilt University Medical Center, 1161 21st Avenue South, Nashville, TN, 37232.ORCID 0000-0003-0460-9377
Vanderbilt University Medical Center · US

Funding

Initiative for Maximizing Student Development (IMSD) at VanderbiltT32GM139800 · NIGMS · VANDERBILT UNIVERSITY · PI RHOADES (STERLING), JULIE A, SEREZANI, C. HENRIQUE · 2021 to 2025
$3.7M
Protection Against Nosocomial Infections After Severe Burn Injury Through Trained ImmunityR35GM141927 · NIGMS · VANDERBILT UNIVERSITY MEDICAL CENTER · PI Julia K. Bohannon · 2021 to 2026
$2.4M
NIGMS NIH HHS T32 GM139800
6 · The paper itself

Abstract

The August 2023 article in Science Signaling, "TGF-β uncouples glycolysis and inflammation in macrophages and controls survival during sepsis," challenges the traditional M1/M2 macrophage classification by investigating the impact of transforming growth factor β on macrophage metabolism and function. Despite its conventional anti-inflammatory role, transforming growth factor β-treated macrophages exhibit a distinct phenotype marked by heightened glycolysis, suppressed proinflammatory cytokines, and increased coagulation factor expression. The study identifies phosphofructokinase, liver type as a crucial glycolytic enzyme regulated by transforming growth factor β via the mTOR-c-MYC pathway. Epigenetic changes induced by transforming growth factor β, such as increased Smad3 activation and reduced proinflammatory transcription factor motif enrichment, contribute to the anti-inflammatory profile. The research extends its implications to sepsis, revealing the role of transforming growth factor β in exacerbating coagulation and reducing survival in mouse models. This effect involves upregulation of coagulation factor F13A1, dependent on phosphofructokinase, liver type activity and glycolysis in macrophages. Connections to COVID-19 pathology are drawn, as transforming growth factor β-treated macrophages and SARS-CoV-2 E protein-exposed cells display similar metabolic profiles. Bioinformatic analysis of COVID-19 patient data suggests correlations between myeloid expression of TGFβR1, PFKL, and F13A1 with disease severity. The study challenges the M1/M2 classification, emphasizing the complexity of macrophage responses influenced by transforming growth factor β, proposing transforming growth factor β as a potential therapeutic target for conditions like sepsis and COVID-19 where dysregulated coagulation is significant. Overall, the research provides valuable insights into transforming growth factor β-mediated immunometabolic regulation, paving the way for future investigations and potential therapeutic interventions.

Indexed as

COVID-19SepsisAnimalsAnti-Inflammatory AgentsBlood Coagulation FactorsHumansMacrophage ActivationMacrophagesMicePhosphofructokinasesTransforming Growth Factor betaAnti-Inflammatory AgentsBlood Coagulation FactorsPhosphofructokinasesTransforming Growth Factor betaimmunometabolisminflammationmacrophagesepsisTGFβ

Identifiers

PMID38197509
PMCPMC11423798
OpenAlexW4390695880

What OpenQuestion holds

Textmetadata
LicenceTDM
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.