Evidence map›Paper›PMID 38092813›Full record

ArticleScientific reports2023

The role of captopril in leukotriene deficient type 1 diabetic mice.

João Pedro Tôrres Guimarães, Luiz A D Queiroz, Kalhara R Menikdiwela, Nayara Pereira, Theresa Ramalho, Sonia Jancar, Naima Moustaid-Moussa, Joilson O Martins

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Scientific reports, 2023. 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
0.4field-weighted citation impact, top 37% 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

1 citing paper in PubMed, 3 citations in OpenAlex.

  1. Cardioprotective Role of Captopril: From Basic to Applied Investigations.International journal of molecular sciences · 2025
    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

8 authors at 4 institutions in 2 countries.

João Pedro Tôrres GuimarãesLaboratory of Immunoendocrinology, School of Pharmaceutical Sciences, Department of Clinical and Toxicological Analyses, University of São Paulo, São Paulo, SP, Brazil.
Luiz A D QueirozLaboratory of Immunoendocrinology, School of Pharmaceutical Sciences, Department of Clinical and Toxicological Analyses, University of São Paulo, São Paulo, SP, Brazil.
Kalhara R MenikdiwelaLaboratory of Nutrigenomics, Inflammation and Obesity Research, Department of Nutritional Sciences, and Obesity Research Institute, Texas Tech University (TTU), Lubbock, TX, USA.
Nayara PereiraLaboratory of Immunopharmacology, Department of Immunology, Institute of Biomedical Sciences, University of São Paulo (ICB/USP), São Paulo, SP, Brazil.
Theresa RamalhoLaboratory of Immunopharmacology, Department of Immunology, Institute of Biomedical Sciences, University of São Paulo (ICB/USP), São Paulo, SP, Brazil.
Sonia JancarLaboratory of Immunopharmacology, Department of Immunology, Institute of Biomedical Sciences, University of São Paulo (ICB/USP), São Paulo, SP, Brazil.
Naima Moustaid-MoussaLaboratory of Nutrigenomics, Inflammation and Obesity Research, Department of Nutritional Sciences, and Obesity Research Institute, Texas Tech University (TTU), Lubbock, TX, USA. naima.moustaid-moussa@ttu.edu.
Joilson O MartinsLaboratory of Immunoendocrinology, School of Pharmaceutical Sciences, Department of Clinical and Toxicological Analyses, University of São Paulo, São Paulo, SP, Brazil. martinsj@usp.br.
Universidade de São Paulo · BRTexas Tech University · USRutgers, The State University of New Jersey · USUniversity of Massachusetts Chan Medical School · US

Funding

Conselho Nacional de Desenvolvimento Científico e Tecnológico 301617/2016-3Conselho Nacional de Desenvolvimento Científico e Tecnológico 310993/2020-2Fundação de Amparo à Pesquisa do Estado de São Paulo 2017/11540-7Fundação de Amparo à Pesquisa do Estado de São Paulo 2018/23266-0Fundação de Amparo à Pesquisa do Estado de São Paulo 2018/50004-6Fundação de Amparo à Pesquisa do Estado de São Paulo 2019/09983-3Fundação de Amparo à Pesquisa do Estado de São Paulo 2020/03175-0Fundação de Amparo à Pesquisa do Estado de São Paulo 2022/00482-4
6 · The paper itself

Abstract

T1D can be associated with metabolic disorders and several impaired pathways, including insulin signaling, and development of insulin resistance through the renin-angiotensin system (RAS). The main precursor of RAS is angiotensinogen (Agt) and this system is often linked to autophagy dysregulation. Dysregulated autophagy has been described in T1D and linked to impairments in both glucose metabolism, and leukotrienes (LTs) production. Here, we have investigated the role of RAS and LTs in both muscle and liver from T1D mice, and its effects on insulin and autophagy pathways. We have chemically induced T1D in 129sve and 129sve 5LO

Indexed as

Diabetes Mellitus, ExperimentalDiabetes Mellitus, Type 1Insulin ResistanceAngiotensinogenAnimalsCaptoprilInsulinLeukotrienesMiceRenin-Angiotensin SystemAngiotensinogenCaptoprilInsulinLeukotrienes

Identifiers

PMID38092813
PMCPMC10719306
OpenAlexW4389711721

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.