Evidence map›Paper›PMID 39407333›Full record

ReviewEuropean journal of medical research2024

Metabolic reprogramming of macrophages in the context of type 2 diabetes.

Leonel Witcoski Junior, Jordana Dinorá de Lima, Amanda Girardi Somensi, Lucas Brito de Souza Santos, Giulia Leonel Paschoal, Thalita Suemy Uada, Thais Sibioni Berti Bastos, André Guilherme Portela de Paula, Rebeca Bosso Dos Santos Luz, Andressa Pacheco Czaikovski and 2 more

Abstract readReview
In one paragraph

Review in European journal of medical research, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
–field-weighted citation impact
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

26 citing papers in PubMed.

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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

12 authors.

Leonel Witcoski JuniorDepartment of Basic Pathology, Federal University of Paraná, Curitiba, PR, Brazil.
Jordana Dinorá de LimaDepartment of Basic Pathology, Federal University of Paraná, Curitiba, PR, Brazil.
Amanda Girardi SomensiDepartment of Genetics, Federal University of Paraná, Curitiba, PR, Brazil.
Lucas Brito de Souza SantosDepartment of Pharmacology, Federal University of Paraná, Curitiba, PR, Brazil.
Giulia Leonel PaschoalMolecular Virology Laboratory, Carlos Chagas Institute, Fiocruz, Curitiba, PR, Brazil.
Thalita Suemy UadaDepartment of Pharmacology, Federal University of Paraná, Curitiba, PR, Brazil.
Thais Sibioni Berti BastosDepartment of Basic Pathology, Federal University of Paraná, Curitiba, PR, Brazil.
André Guilherme Portela de PaulaDepartment of Basic Pathology, Federal University of Paraná, Curitiba, PR, Brazil.
Rebeca Bosso Dos Santos LuzDepartment of Basic Pathology, Federal University of Paraná, Curitiba, PR, Brazil.
Andressa Pacheco CzaikovskiDepartment of Basic Pathology, Federal University of Paraná, Curitiba, PR, Brazil.
Mariana Rodrigues DavansoTuiuti University of Parana, Curitiba, PR, Brazil.
Tarcio Teodoro BragaDepartment of Basic Pathology, Federal University of Paraná, Curitiba, PR, Brazil. tarcio.braga@ufpr.br.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Type 2 diabetes (T2D) is associated with insulin resistance and progressive dysfunction of β-pancreatic cells, leading to persistent hyperglycemia. Macrophages play a crucial role in this context, influencing both the development and progression of insulin resistance. These innate immune cells respond to inflammatory stimuli and reprogram their metabolism, directly impacting the pathophysiology of T2D. Macrophages are highly plastic and can adopt either pro-inflammatory or pro-resolutive phenotypic profiles. In T2D, pro-inflammatory macrophages, which rely on glycolysis, exacerbate insulin resistance through increased production of pro-inflammatory cytokines and nitric oxide. In contrast, pro-resolutive macrophages, which prioritize fatty acid metabolism, have different effects on glucose homeostasis. Metaflammation, a chronic low-grade inflammation, is induced by pro-inflammatory macrophages and significantly contributes to the progression of T2D, creating an environment conducive to metabolic dysfunction. This review aims to clarify the contribution of macrophages to the progression of T2D by detailing how their inflammatory responses and metabolic reprogramming influence insulin resistance and the disease's pathophysiology. The review seeks to deepen the understanding of the biochemical and metabolic mechanisms involved, offering broader insights into the impact on the quality of life for millions of patients worldwide.

Indexed as

Diabetes Mellitus, Type 2Insulin ResistanceMacrophagesAnimalsCellular ReprogrammingHumansInflammationMetabolic ReprogrammingEpigenetic modificationsImmunometabolismMacrophageT2D

Identifiers

PMID39407333
PMCPMC11481356

What OpenQuestion holds

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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.