Evidence map›Paper›PMID 27199111›Full record

ArticleAmerican journal of physiology. Heart and circulatory physiology2016

Discordant signaling and autophagy response to fasting in hearts of obese mice: Implications for ischemia tolerance.

Allen M Andres, Joel A Kooren, Sarah J Parker, Kyle C Tucker, Nandini Ravindran, Bruce R Ito, Chengqun Huang, Vidya Venkatraman, Jennifer E Van Eyk, Roberta A Gottlieb and 1 more

Open access · bronzeAbstract read
In one paragraph

Article in American journal of physiology. Heart and circulatory physiology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed, 1 pooled it
3.6field-weighted citation impact, top 7% 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

23 citing papers in PubMed, 1 synthesis or guideline pooled it, 35 citations in OpenAlex.

  1. Guidelines for experimental models of myocardial ischemia and infarction.American journal of physiology. Heart and circulatory physiology · 2018
    Guideline
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  14. Decrease of Cardiac Parkin Protein in Obese Mice.Frontiers in cardiovascular medicine · 2019
    Article
  15. Cardiac revascularization: state of the art and perspectives.Vascular biology (Bristol, England) · 2019
    Review
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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

11 authors at 3 institutions in 1 country.

Allen M AndresCedars-Sinai Heart Institute and Department of Medicine, Los Angeles, California; Barbra Streisand Women's Heart Center of Cedars-Sinai Medical Center, Los Angeles, California; and Allen.Andres@cshs.org.
Joel A KoorenCedars-Sinai Heart Institute and Department of Medicine, Los Angeles, California; Barbra Streisand Women's Heart Center of Cedars-Sinai Medical Center, Los Angeles, California; and.
Sarah J ParkerCedars-Sinai Heart Institute and Department of Medicine, Los Angeles, California; Barbra Streisand Women's Heart Center of Cedars-Sinai Medical Center, Los Angeles, California; and.
Kyle C TuckerCedars-Sinai Heart Institute and Department of Medicine, Los Angeles, California; Barbra Streisand Women's Heart Center of Cedars-Sinai Medical Center, Los Angeles, California; and.
Nandini RavindranDonald P. Shiley BioScience Center, San Diego State University, San Diego, California.
Bruce R ItoDonald P. Shiley BioScience Center, San Diego State University, San Diego, California.
Chengqun HuangCedars-Sinai Heart Institute and Department of Medicine, Los Angeles, California; Barbra Streisand Women's Heart Center of Cedars-Sinai Medical Center, Los Angeles, California; and.
Vidya VenkatramanCedars-Sinai Heart Institute and Department of Medicine, Los Angeles, California; Barbra Streisand Women's Heart Center of Cedars-Sinai Medical Center, Los Angeles, California; and.
Jennifer E Van EykCedars-Sinai Heart Institute and Department of Medicine, Los Angeles, California; Barbra Streisand Women's Heart Center of Cedars-Sinai Medical Center, Los Angeles, California; and.
Roberta A GottliebCedars-Sinai Heart Institute and Department of Medicine, Los Angeles, California; Barbra Streisand Women's Heart Center of Cedars-Sinai Medical Center, Los Angeles, California; and.
Robert M MentzerCedars-Sinai Heart Institute and Department of Medicine, Los Angeles, California; Barbra Streisand Women's Heart Center of Cedars-Sinai Medical Center, Los Angeles, California; and.
Cedars-Sinai Smidt Heart Institute · USCedars-Sinai Medical Center · USSan Diego State University · US

Funding

Protein Chemistry and ProteomicsP01HL112730 · NHLBI · SAN DIEGO STATE UNIVERSITY · PI VAN EYK, JENNIFER E · 2013 to 2017
$12.0M
NHLBI NIH HHS P01 HL112730
6 · The paper itself

Abstract

Autophagy is regulated by nutrient and energy status and plays an adaptive role during nutrient deprivation and ischemic stress. Metabolic syndrome (MetS) is a hypernutritive state characterized by obesity, dyslipidemia, elevated fasting blood glucose levels, and insulin resistance. It has also been associated with impaired autophagic flux and larger-sized infarcts. We hypothesized that diet-induced obesity (DIO) affects nutrient sensing, explaining the observed cardiac impaired autophagy. We subjected male friend virus B NIH (FVBN) mice to a high-fat diet, which resulted in increased weight gain, fat deposition, hyperglycemia, insulin resistance, and larger infarcts after myocardial ischemia-reperfusion. Autophagic flux was impaired after 4 wk on a high-fat diet. To interrogate nutrient-sensing pathways, DIO mice were subjected to overnight fasting, and hearts were processed for biochemical and proteomic analysis. Obese mice failed to upregulate LC3-II or to clear p62/SQSTM1 after fasting, although mRNA for LC3B and p62/SQSTM1 were appropriately upregulated in both groups, demonstrating an intact transcriptional response to fasting. Energy- and nutrient-sensing signal transduction pathways [AMPK and mammalian target of rapamycin (mTOR)] also responded appropriately to fasting, although mTOR was more profoundly suppressed in obese mice. Proteomic quantitative analysis of the hearts under fed and fasted conditions revealed broad changes in protein networks involved in oxidative phosphorylation, autophagy, oxidative stress, protein homeostasis, and contractile machinery. In many instances, the fasting response was quite discordant between lean and DIO mice. Network analysis implicated the peroxisome proliferator-activated receptor and mTOR regulatory nodes. Hearts of obese mice exhibited impaired autophagy, altered proteome, and discordant response to nutrient deprivation.

Indexed as

AutophagyAMP-Activated Protein KinasesAnimalsDiet, High-FatDisease Models, AnimalEnergy MetabolismFastingMaleMetabolic SyndromeMiceMicrotubule-Associated ProteinsMyocardial InfarctionMyocardial Reperfusion InjuryMyocardiumObesityPeroxisome Proliferator-Activated ReceptorsAMP-Activated Protein KinasesMap1lc3b protein, mouseMicrotubule-Associated ProteinsmTOR protein, mousePeroxisome Proliferator-Activated ReceptorsSequestosome-1 ProteinSqstm1 protein, mouseTOR Serine-Threonine Kinasesmammalian target of rapamycinmetabolic syndromeperoxisome proliferator-activated receptor-α/γproteomics

Identifiers

PMID27199111
PMCPMC4967197
OpenAlexW2346567573

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.