Evidence map›Paper›PMID 29196345›Full record

ArticleAmerican journal of physiology. Heart and circulatory physiology2018

Mitoprotection attenuates myocardial vascular impairment in porcine metabolic syndrome.

Fang Yuan, Ahmad F Hedayat, Christopher M Ferguson, Amir Lerman, Lilach O Lerman, Alfonso Eirin

Open access · bronzeAbstract read
In one paragraph

Article in American journal of physiology. Heart and circulatory physiology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
1.6field-weighted citation impact, top 14% 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

15 citing papers in PubMed, 20 citations in OpenAlex.

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  14. Enhancing Mitochondrial Health to Treat Hypertension.Current hypertension reports · 2018
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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

6 authors at 3 institutions in 2 countries.

Fang YuanDivision of Nephrology and Hypertension, Mayo Clinic , Rochester, Minnesota.
Ahmad F HedayatDivision of Nephrology and Hypertension, Mayo Clinic , Rochester, Minnesota.
Christopher M FergusonDivision of Nephrology and Hypertension, Mayo Clinic , Rochester, Minnesota.
Amir LermanDepartment of Cardiovascular Diseases, Mayo Clinic , Rochester, Minnesota.
Lilach O LermanDivision of Nephrology and Hypertension, Mayo Clinic , Rochester, Minnesota.
Alfonso EirinDivision of Nephrology and Hypertension, Mayo Clinic , Rochester, Minnesota.
Mayo Clinic · USWinnMed · USHenan Provincial People's Hospital · CN

Funding

A potential role for mitoprotection in preserving the kidney in metabolic syndrome and renal artery stenosisK08DK106427 · NIDDK · MAYO CLINIC ROCHESTER · PI EIRIN, ALFONSO · 2015 to 2019
$819k
NIDDK NIH HHS K08 DK106427
6 · The paper itself

Abstract

Metabolic syndrome (MetS) leads to cardiac vascular injury, which may reflect in increased retention of endothelial progenitor cells (EPCs). Coronary endothelial cell (EC) mitochondria partly regulate vascular function and structure. We hypothesized that chronic mitoprotection would preserve EC mitochondria and attenuate coronary vascular injury and dysfunction in swine MetS. Pigs were studied after 16 wk of diet-induced MetS, MetS treated for the last 4 wk with the mitochondria-targeted peptide elamipretide (ELAM; 0.1 mg/kg sc once daily), and lean controls ( n = 6 each). Cardiac remodeling and function were assessed in vivo by multidetector-computed tomography (CT), and coronary artery and sinus blood samples were collected. EC mitochondrial density, apoptosis, oxidative stress, endothelial nitric oxide synthase immunoreactivity, myocardial microvascular density (three-dimensional microcomputed tomography), and coronary endothelial function (organ bath) were assessed ex vivo. The number and arteriovenous gradient of CD34

Indexed as

AnimalsApoptosisCoronary Artery DiseaseCoronary VesselsCytoprotectionDisease Models, AnimalEndothelial Progenitor CellsEndothelium, VascularFemaleMetabolic SyndromeMitochondriaNeovascularization, PhysiologicNitric Oxide Synthase Type IIIOligopeptidesOxidative StressProtective Agentsarginyl-2,'6'-dimethyltyrosyl-lysyl-phenylalaninamideNitric Oxide Synthase Type IIIOligopeptidesProtective Agentselamipretidemetabolic syndromemicrovesselsmitochondriamyocardium

Identifiers

PMID29196345
PMCPMC5899259
OpenAlexW2773051492

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.