Evidence map›Paper›PMID 29331057›Full record

ReviewJournal of internal medicine2018

Manifestations and mechanisms of myocardial lipotoxicity in obesity.

A C Sletten, L R Peterson, J E Schaffer

Open access · bronzeAbstract readReview
In one paragraph

Review in Journal of internal medicine, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 87 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
87citing papers in PubMed, 1 pooled it
7.1field-weighted citation impact, top 2% 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

87 citing papers in PubMed, 1 synthesis or guideline pooled it, 131 citations in OpenAlex.

  1. Pooled it
  2. Trial
  3. Trial
  4. Article
  5. Article
  6. Review
  7. Article
  8. Review
  9. Review
  10. Review
  11. Article
  12. Review
  13. Article
  14. Article
  15. Review
  16. Article
  17. Review
  18. Review
  19. Article
  20. Article

27 more citing papers are in PubMed but not listed here.

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

3 authors at 1 institution in 1 country.

A C SlettenDepartment of Medicine, Washington University, St Louis, MO, USA.
L R PetersonDepartment of Medicine, Washington University, St Louis, MO, USA.
J E SchafferDepartment of Medicine, Washington University, St Louis, MO, USA.ORCID 0000-0002-4954-6659
Washington University in St. Louis · US

Funding

WU INSTITUTE OF CLINICAL AND TRANSLATIONAL SCIENCESUL1TR002345 · NCATS · WASHINGTON UNIVERSITY · PI William G. Powderly · 2017 to 2026
$97.8M
WU P&FP30DK020579 · NIDDK · WASHINGTON UNIVERSITY · PI Irfan J Lodhi · 2013 to 2026
$27.1M
CELLULAR MECHANISMS THAT PROMOTE OR PREVENT LIPOTOXICITYR01DK064989 · NIDDK · WASHINGTON UNIVERSITY · PI SCHAFFER, JEAN E. · 2003 to 2021
$5.8M
Lipid Biomarkers for Diabetic Heart DiseaseP20HL113444 · NHLBI · WASHINGTON UNIVERSITY · PI SCHAFFER, JEAN E. · 2012 to 2016
$4.7M
THE INORGANIC NITRATE FOR EXERCISE IN HEART FAILURE (INIX-HF) TRIALR34HL138253 · NHLBI · WASHINGTON UNIVERSITY · PI COGGAN, ANDREW R, PETERSON, LINDA RUTH · 2017 to 2019
$701k
NCATS NIH HHS UL1 TR002345NHLBI NIH HHS P20 HL113444NHLBI NIH HHS R34 HL138253NIDDK NIH HHS P30 DK020579NIDDK NIH HHS R01 DK064989
6 · The paper itself

Abstract

Environmental and socioeconomic changes over the past thirty years have contributed to a dramatic rise in the worldwide prevalence of obesity. Heart disease is amongst the most serious health risks of obesity, with increases in both atherosclerotic coronary heart disease and heart failure among obese individuals. In this review, we focus on primary myocardial alterations in obesity that include hypertrophic remodelling and diastolic dysfunction. Obesity-associated perturbations in myocardial and systemic lipid metabolism are important contributors to cardiovascular complications of obesity. Accumulation of excess lipid in nonadipose cells of the cardiovascular system can cause cell dysfunction and cell death, a process known as lipotoxicity. Lipotoxicity has been modelled in mice using high-fat diet feeding, inbred lines with mutations in leptin receptor signalling, and in genetically engineered mice with enhanced myocardial fatty acid uptake, altered lipid droplet homoeostasis or decreased cardiac fatty acid oxidation. These studies, along with findings in cell culture model systems, indicate that the molecular pathophysiology of lipid overload involves endoplasmic reticulum stress, alterations in autophagy, de novo ceramide synthesis, oxidative stress, inflammation and changes in gene expression. We highlight recent advances that extend our understanding of the impact of obesity and altered lipid metabolism on cardiac function.

Indexed as

Lipid MetabolismAnimalsCardiomyopathiesHumansMyocardiumObesitydiabetesheart failurelipidsobesity

Identifiers

PMID29331057
PMCPMC6045461
OpenAlexW2783821648

What OpenQuestion holds

Textmetadata
LicenceTDM
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.