Evidence map›Paper›PMID 39605858›Full record

ArticleFrontiers in physiology2024

A sex-dependent role of Kv1.3 channels from macrophages in metabolic syndrome.

Diego A Peraza, Lucía Benito-Salamanca, Sara Moreno-Estar, Esperanza Alonso, José R López-López, M Teresa Pérez-Garcia, Pilar Cidad

Abstract read
In one paragraph

Article in Frontiers in physiology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing 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

1 citing paper in PubMed.

  1. Article
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

7 authors.

Diego A PerazaDepartamento de Bioquímica y Biología Molecular y Fisiología, Universidad de Valladolid, Valladolid, Spain.
Lucía Benito-SalamancaDepartamento de Bioquímica y Biología Molecular y Fisiología, Universidad de Valladolid, Valladolid, Spain.
Sara Moreno-EstarDepartamento de Bioquímica y Biología Molecular y Fisiología, Universidad de Valladolid, Valladolid, Spain.
Esperanza AlonsoDepartamento de Bioquímica y Biología Molecular y Fisiología, Universidad de Valladolid, Valladolid, Spain.
José R López-López *Departamento de Bioquímica y Biología Molecular y Fisiología, Universidad de Valladolid, Valladolid, Spain.
M Teresa Pérez-Garcia *Departamento de Bioquímica y Biología Molecular y Fisiología, Universidad de Valladolid, Valladolid, Spain.
Pilar Cidad *Departamento de Bioquímica y Biología Molecular y Fisiología, Universidad de Valladolid, Valladolid, Spain.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Introduction: Coronary artery disease (CAD) is the foremost single cause of mortality and disability globally. Patients with type 2 diabetes (T2DM) have a higher incidence of CAD, and poorer prognosis. The low-grade inflammation associated to T2DM contributes to increased morbidity and worst outcomes after revascularization. Inflammatory signaling in the vasculature supports endothelial dysfunction, leukocyte infiltration, and macrophage activation to a metabolic disease (MMe) specific phenotype, which could contribute to the metabolic disorders and ascular damage in T2DM. We have previously found that K Methods and Results: Male and female BPH mice fed on high-fat diet (HFD) develop metabolic syndrome (MetS) and T2DM. mRNA levels of several K Conclusion: Altogether, our data suggest that by inhibiting macrophage infiltration, Kv1.3 blockers could contribute to disrupt the vicious cycle of inflammation and insulin resistance, offering a novel approach to prevent MetS, T2DM and its associated cardiovascular complications in females.

Indexed as

bone marrow-derived macrophagescell migrationelectrophysiologyKv1.3 channelsmacrophage phenotypemetabolic syndromesex-dependent differences

Identifiers

PMID39605858
PMCPMC11599228

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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.