Evidence map›Paper›PMID 31572553›Full record

ArticleExperimental and therapeutic medicine2019

Aminoguanidine reduces diabetes-associated cardiac fibrosis.

Fernando Magdaleno, Chuck Christopher Blajszczak, Claudia Lisette Charles-Niño, Alma Marlene Guadrón-Llanos, Alan Omar Vázquez-Álvarez, Alejandra Guillermina Miranda-Díaz, Natalia Nieto, María Cristina Islas-Carbajal, Ana Rosa Rincón-Sánchez

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

Article in Experimental and therapeutic medicine, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
1.4field-weighted citation impact, top 22% 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

13 citing papers in PubMed, 21 citations in OpenAlex.

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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

9 authors at 2 institutions in 2 countries.

Fernando MagdalenoDepartment of Physiology, University Center of Health Sciences, Guadalajara University, Guadalajara, Jalisco 44340, Mexico.
Chuck Christopher BlajszczakDepartment of Pathology, College of Medicine, University of Illinois at Chicago, IL 60612, USA.
Claudia Lisette Charles-NiñoDepartment of Physiology, University Center of Health Sciences, Guadalajara University, Guadalajara, Jalisco 44340, Mexico.
Alma Marlene Guadrón-LlanosDepartment of Physiology, University Center of Health Sciences, Guadalajara University, Guadalajara, Jalisco 44340, Mexico.
Alan Omar Vázquez-ÁlvarezDepartment of Physiology, University Center of Health Sciences, Guadalajara University, Guadalajara, Jalisco 44340, Mexico.
Alejandra Guillermina Miranda-DíazInstitute of Experimental and Clinical Therapeutics, Department of Physiology, University Center of Health Sciences, Guadalajara University, Guadalajara, Jalisco 44340, Mexico.
Natalia NietoDepartment of Pathology, College of Medicine, University of Illinois at Chicago, IL 60612, USA.
María Cristina Islas-CarbajalInstitute of Experimental and Clinical Therapeutics, Department of Physiology, University Center of Health Sciences, Guadalajara University, Guadalajara, Jalisco 44340, Mexico.
Ana Rosa Rincón-SánchezInstitute of Molecular Biology and Gene Therapy, Department of Molecular Biology and Genomics, University Center of Health Sciences, Guadalajara University, Guadalajara, Jalisco 44340, Mexico.
Universidad de Guadalajara · MXUniversity of Illinois Chicago · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Aminoguanidine (AG) inhibits advanced glycation end products (AGEs) and advanced oxidation protein products (AOPP) accumulated as a result of excessive oxidative stress in diabetes. However, the molecular mechanism by which AG reduces AGE-associated damage in diabetes is not well understood. Thus, we investigated whether AG supplementation mitigates oxidative-associated cardiac fibrosis in rats with type 2 diabetes mellitus (T2DM). Forty-five male Wistar rats were divided into three groups: Control, T2DM and T2DM+AG. Rats were fed with a high-fat, high-carbohydrate diet (HFCD) for 2 weeks and rendered diabetic using low-dose streptozotocin (STZ) (20 mg/kg), and one group was treated with AG (20 mg/kg) up to 25 weeks.

Indexed as

AGAGEscardiac fibrosiscollagen type Idiabetesoxidative stressRAGESTZ

Identifiers

PMID31572553
PMCPMC6755450
OpenAlexW2969898469

What OpenQuestion holds

Textmetadata
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.