Evidence map›Paper›PMID 38116319›Full record

ArticleFrontiers in endocrinology2023

Low glucose availability potentiates the effects of metformin on model T cell activation and exhaustion markers

Jernej Repas, Lea Peternel, Harald Sourij, Mojca Pavlin

Open access · goldAbstract read
In one paragraph

Article in Frontiers in endocrinology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
1.4field-weighted citation impact, top 18% 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

9 citing papers in PubMed, 9 citations in OpenAlex.

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  9. CD8Frontiers in immunology · 2024
    Review
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

4 authors at 2 institutions in 2 countries.

Jernej RepasInstitute of Biophysics, Faculty of Medicine, University of Ljubljana, Ljubljana, Slovenia.
Lea PeternelInstitute of Biophysics, Faculty of Medicine, University of Ljubljana, Ljubljana, Slovenia.
Harald SourijTrials Unit for Interdisciplinary Metabolic Medicine, Division of Endocrinology and Diabetology, Medical University Graz, Graz, Austria.
Mojca PavlinInstitute of Biophysics, Faculty of Medicine, University of Ljubljana, Ljubljana, Slovenia.
University of Ljubljana · SIMedical University of Graz · AT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Modulation of immune cell metabolism is one of promising strategies to improve cancer immunotherapies. Metformin is an anti-diabetic drug with potential anti-cancer effects, ranging from normalization of blood glucose and insulin levels, direct anti-proliferative effects on cancer cells to emerging immunomodulatory effects on anti-tumor immunity. Metformin can reduce tumor hypoxia and PD-L1 expression, as well as normalize or improve T cell function and potentiate the effect of immune checkpoint inhibitors, making it a promising adjuvant to immunotherapy of tumors with poor response such as triple negative breast cancer (TNBC). However, although the effects of metformin on cancer cells are glucose-dependent, the role of glucose in modulating its effect on T cells has not been systematically studied. We thus investigated the effect of metformin as a function of glucose level on Jurkat cell and PBMC T cell models

Indexed as

MetforminGlucoseHumansLeukocytes, MononuclearProgrammed Cell Death 1 ReceptorT-LymphocytesGlucoseMetforminProgrammed Cell Death 1 Receptor2-deoxy-D-glucoseglucose levelmetforminPD-1/PD-L1 axisT cell exhaustionT cells

Identifiers

PMID38116319
PMCPMC10728603
OpenAlexW4389344914

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.