Evidence map›Paper›PMID 28646024›Full record

ReviewAmerican journal of physiology. Heart and circulatory physiology2017

Metabolic reprogramming via PPARα signaling in cardiac hypertrophy and failure: From metabolomics to epigenetics.

Junco Shibayama Warren, Shin-Ichi Oka, Daniela Zablocki, Junichi Sadoshima

Open access · bronzeAbstract readReview
In one paragraph

Review in American journal of physiology. Heart and circulatory physiology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
41citing papers in PubMed, 1 pooled it
3.4field-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

41 citing papers in PubMed, 1 synthesis or guideline pooled it, 63 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Article
  4. Article
  5. Review
  6. Review
  7. Article
  8. Review
  9. Review
  10. Review
  11. Article
  12. Article
  13. Article
  14. Application of 4-D ultrasound-derived regional strain and proteomics analysis inAmerican journal of physiology. Heart and circulatory physiology · 2023
    Article
  15. [Molecular pathological mechanism of liver metabolic disorder in mice with severe spinal muscular atrophy].Nan fang yi ke da xue xue bao = Journal of Southern Medical University · 2023
    Article
  16. Review
  17. Review
  18. Article
  19. Article
  20. 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

4 authors at 2 institutions in 1 country.

Junco Shibayama WarrenNora Eccles Harrison Cardiovascular Research and Training Institute, University of Utah, Salt Lake City, Utah; junco.warren@utah.edu.ORCID http://orcid.org/0000-0001-5231-4181
Shin-Ichi OkaDepartment of Cell Biology and Molecular Medicine, Rutgers New Jersey Medical School, Newark, New Jersey.
Daniela ZablockiDepartment of Cell Biology and Molecular Medicine, Rutgers New Jersey Medical School, Newark, New Jersey.
Junichi SadoshimaDepartment of Cell Biology and Molecular Medicine, Rutgers New Jersey Medical School, Newark, New Jersey.
Rutgers, The State University of New Jersey · USUniversity of Utah · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Studies using omics-based approaches have advanced our knowledge of metabolic remodeling in cardiac hypertrophy and failure. Metabolomic analysis of the failing heart has revealed global changes in mitochondrial substrate metabolism. Peroxisome proliferator-activated receptor-α (PPARα) plays a critical role in synergistic regulation of cardiac metabolism through transcriptional control. Metabolic reprogramming via PPARα signaling in heart failure ultimately propagates into myocardial energetics. However, emerging evidence suggests that the expression level of PPARα per se does not always explain the energetic state in the heart. The transcriptional activities of PPARα are dynamic, yet highly coordinated. An additional level of complexity in the PPARα regulatory mechanism arises from its ability to interact with various partners, which ultimately determines the metabolic phenotype of the diseased heart. This review summarizes our current knowledge of the PPARα regulatory mechanisms in cardiac metabolism and the possible role of PPARα in epigenetic modifications in the diseased heart. In addition, we discuss how metabolomics can contribute to a better understanding of the role of PPARα in the progression of cardiac hypertrophy and failure.

Indexed as

Energy MetabolismEpigenesis, GeneticMetabolomicsTranscription, GeneticAnimalsCardiomegalyDisease ProgressionEpigenomicsHeart FailureHumansMyocardiumPPAR gammaSignal TransductionPPAR gammadeoxyribonucleotidefatty acidsmetabolismperoxisome proliferator-activated receptor-α

Identifiers

PMID28646024
PMCPMC6425516
OpenAlexW2680144180

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.