Evidence map›Paper›PMID 32804947›Full record

ArticlePloS one2020

The evolving systemic biomarker milieu in obese ZSF1 rat model of human cardiometabolic syndrome: Characterization of the model and cardioprotective effect of GDF15.

Marina Stolina, Xin Luo, Denise Dwyer, Chun-Ya Han, Rhonda Chen, Ying Zhang, YuMei Xiong, Yinhong Chen, Jun Yin, Artem Shkumatov and 3 more

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing 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

18 citing papers in PubMed, 28 citations in OpenAlex.

  1. Article
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  10. Adjunctive therapy with an oral HBritish journal of pharmacology · 2024
    Article
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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

13 authors at 1 institution in 1 country.

Marina StolinaAmgen Research, Department of Cardiometabolic, Thousand Oaks, California, United States of America.
Xin LuoAmgen Research, Genome Analysis Unit, San Francisco, California, United States of America.
Denise DwyerAmgen Research, Department of Cardiometabolic, Thousand Oaks, California, United States of America.
Chun-Ya HanAmgen Research, Department of Cardiometabolic, Thousand Oaks, California, United States of America.
Rhonda ChenAmgen Research, Department of Cardiometabolic, San Francisco, California, United States of America.
Ying ZhangAmgen Research, Department of Cardiometabolic, San Francisco, California, United States of America.
YuMei XiongAmgen Research, Department of Cardiometabolic, San Francisco, California, United States of America.
Yinhong ChenAmgen Research, Department of Cardiometabolic, San Francisco, California, United States of America.
Jun YinAmgen Research, Genome Analysis Unit, San Francisco, California, United States of America.
Artem ShkumatovAmgen Research, Department of Translational and Bioanalytical Sciences, San Francisco, California, United States of America.
Brandon AsonAmgen Research, Department of Cardiometabolic, San Francisco, California, United States of America.
Clarence HaleAmgen Research, Department of Cardiometabolic, Thousand Oaks, California, United States of America.
Murielle M VéniantAmgen Research, Department of Cardiometabolic, Thousand Oaks, California, United States of America.ORCID 0000-0002-1881-8252
Amgen (United States) · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cardiometabolic syndrome has become a global health issue. Heart failure is a common comorbidity of cardiometabolic syndrome. Successful drug development to prevent cardiometabolic syndrome and associated comorbidities requires preclinical models predictive of human conditions. To characterize the heart failure component of cardiometabolic syndrome, cardiometabolic, metabolic, and renal biomarkers were evaluated in lean and obese ZSF1 19- to 32-week-old male rats. Histopathological assessment of kidneys and hearts was performed. Cardiac function, exercise capacity, and left ventricular gene expression were also analyzed. Obese ZSF1 rats exhibited multiple features of human cardiometabolic syndrome by pathological changes in systemic renal, metabolic, and cardiovascular disease circulating biomarkers. Hemodynamic assessment, echocardiography, and decreased exercise capacity confirmed heart failure with preserved ejection fraction. RNA-seq results demonstrated changes in left ventricular gene expression associated with fatty acid and branched chain amino acid metabolism, cardiomyopathy, cardiac hypertrophy, and heart failure. Twelve weeks of growth differentiation factor 15 (GDF15) treatment significantly decreased body weight, food intake, blood glucose, and triglycerides and improved exercise capacity in obese ZSF1 males. Systemic cardiovascular injury markers were significantly lower in GDF15-treated obese ZSF1 rats. Obese ZSF1 male rats represent a preclinical model for human cardiometabolic syndrome with established heart failure with preserved ejection fraction. GDF15 treatment mediated dietary response and demonstrated a cardioprotective effect in obese ZSF1 rats.

Indexed as

AnimalsBiomarkersGrowth Differentiation Factor 15HeartHeart FailureHeart VentriclesKidneyMaleMetabolic SyndromeMyocardiumObesityRatsRats, Inbred StrainsRats, ZuckerStroke VolumeVentricular Function, LeftBiomarkersGrowth Differentiation Factor 15

Identifiers

PMID32804947
PMCPMC7430742
OpenAlexW3050470919

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.