Evidence map›Paper›PMID 26766185›Full record

ArticlePloS one2016

Early Cellular Changes in the Ascending Aorta and Myocardium in a Swine Model of Metabolic Syndrome.

Rabya Saraf, Thomas Huang, Feroze Mahmood, Khurram Owais, Amit Bardia, Kamal R Khabbaz, David Liu, Venkatachalam Senthilnathan, Antonio D Lassaletta, Frank Sellke and 1 more

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2016. 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
0.2field-weighted citation impact, top 39% 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, 5 citations in OpenAlex.

  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

11 authors at 3 institutions in 1 country.

Rabya SarafDepartment of Surgery, Division of Cardiac Surgery, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, Massachusetts, United States of America.
Thomas HuangDepartment of Anesthesia, Critical Care and Pain Medicine, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, Massachusetts, United States of America.
Feroze MahmoodDepartment of Anesthesia, Critical Care and Pain Medicine, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, Massachusetts, United States of America.
Khurram OwaisDepartment of Anesthesia, Critical Care and Pain Medicine, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, Massachusetts, United States of America.
Amit BardiaDepartment of Anesthesia, Critical Care and Pain Medicine, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, Massachusetts, United States of America.
Kamal R KhabbazDepartment of Surgery, Division of Cardiac Surgery, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, Massachusetts, United States of America.
David LiuDepartment of Surgery, Division of Cardiac Surgery, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, Massachusetts, United States of America.
Venkatachalam SenthilnathanDepartment of Surgery, Division of Cardiac Surgery, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, Massachusetts, United States of America.
Antonio D LassalettaDepartment of Surgery, Division of Cardiac Surgery, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, Massachusetts, United States of America.
Frank SellkeDepartment of Surgery, Rhode Island Hospital, Brown Alpert School of Medicine, Providence, Rhode Island, United States of America.
Robina MatyalDepartment of Anesthesia, Critical Care and Pain Medicine, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, Massachusetts, United States of America.
Harvard University · USBeth Israel Deaconess Medical Center · USRhode Island Hospital · US

Funding

Effect of Cardioplegia and Cardiopulmonary Bypass on Coronary Microvascular ReactivityR01HL046716 · NHLBI · RHODE ISLAND HOSPITAL · PI SELLKE, FRANK W · 1997 to 2023
$8.5M
Surgical Intramyocardial Angiogenesis in a Swine Model of Endothelial DysfunctionR01HL069024 · NHLBI · RHODE ISLAND HOSPITAL · PI SELLKE, FRANK W · 2002 to 2011
$3.7M
NHLBI NIH HHS R01 HL046716NHLBI NIH HHS R01 HL069024NHLBI NIH HHS R01 HL46716
6 · The paper itself

Abstract

backgroundMetabolic syndrome is associated with pathological remodeling of the heart and adjacent vessels. The early biochemical and cellular changes underlying the vascular damage are not fully understood. In this study, we sought to establish the nature, extent, and initial timeline of cytochemical derangements underlying reduced ventriculo-arterial compliance in a swine model of metabolic syndrome.

methodsYorkshire swine (n = 8 per group) were fed a normal diet (ND) or a high-cholesterol (HCD) for 12 weeks. Myocardial function and blood flow was assessed before harvesting the heart. Immuno-blotting and immuno-histochemical staining were used to assess the cellular changes in the myocardium, ascending aorta and left anterior descending artery (LAD).

resultsThere was significant increase in body mass index, blood glucose and mean arterial pressures (p = 0.002, p = 0.001 and p = 0.024 respectively) in HCD group. At the cellular level there was significant increase in anti-apoptotic factors p-Akt (p = 0.007 and p = 0.002) and Bcl-xL (p = 0.05 and p = 0.01) in the HCD aorta and myocardium, respectively. Pro-fibrotic markers TGF-β (p = 0.01), pSmad1/5 (p = 0.03) and MMP-9 (p = 0.005) were significantly increased in the HCD aorta. The levels of pro-apoptotic p38MAPK, Apaf-1 and cleaved Caspase3 were significantly increased in aorta of HCD (p = 0.03, p = 0.04 and p = 0.007 respectively). Similar changes in coronary arteries were not observed in either group. Functionally, the high cholesterol diet resulted in significant increase in ventricular end systolic pressure and-dp/dt (p = 0.05 and p = 0.007 respectively) in the HCD group.

conclusionPreclinical metabolic syndrome initiates pro-apoptosis and pro-fibrosis pathways in the heart and ascending aorta, while sparing coronary arteries at this early stage of dietary modification.

Indexed as

AnimalsAortaApoptosisApoptotic Protease-Activating Factor 1Caspase 3Diet, High-FatFibrosisMetabolic SyndromeMyocardiump38 Mitogen-Activated Protein KinasesSmad1 ProteinSwineTransforming Growth Factor betaApoptotic Protease-Activating Factor 1Caspase 3p38 Mitogen-Activated Protein KinasesSmad1 ProteinTransforming Growth Factor beta

Identifiers

PMID26766185
PMCPMC4713205
OpenAlexW2237579606

What OpenQuestion holds

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LicenceCC BY
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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.