Evidence map›Paper›PMID 27742689›Full record

ReviewAmerican journal of physiology. Heart and circulatory physiology2017

Role of microRNA in metabolic shift during heart failure.

Mark V Pinti, Quincy A Hathaway, John M Hollander

Open access · greenAbstract 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 37 papers.

0numbers the graph read from it
0cells of the map it votes in
37citing papers in PubMed
3.5field-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

37 citing papers in PubMed, 59 citations in OpenAlex.

  1. Review
  2. Review
  3. Review
  4. Article
  5. Article
  6. Review
  7. Mitochondrial microRNAs Are Dysregulated in Patients with Fabry Disease.The Journal of pharmacology and experimental therapeutics · 2023
    Article
  8. Cardiac Metabolism and MiRNA Interference.International journal of molecular sciences · 2022
    Review
  9. Article
  10. Review
  11. Review
  12. Review
  13. Article
  14. Review
  15. Article
  16. Review
  17. Review
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  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

3 authors at 1 institution in 1 country.

Mark V PintiDivision of Exercise Physiology, West Virginia University School of Medicine, Morgantown, West Virginia; and Mitochondria, Metabolism, and Bioenergentics Working Group, Morgantown, West Virginia.
Quincy A HathawayDivision of Exercise Physiology, West Virginia University School of Medicine, Morgantown, West Virginia; and Mitochondria, Metabolism, and Bioenergentics Working Group, Morgantown, West Virginia.
John M HollanderDivision of Exercise Physiology, West Virginia University School of Medicine, Morgantown, West Virginia; and Mitochondria, Metabolism, and Bioenergentics Working Group, Morgantown, West Virginia jhollander@hsc.wvu.edu.
West Virginia University · US

Funding

WV INBRE: The Inhibitor of Growth Family Member 4 (ING4) inhibits L-Type Amino Acid Transporter 1 (LAT1) expression to suppress Breast CancerP20GM103434 · NIGMS · MARSHALL UNIVERSITY · PI GARY O RANKIN · 2012 to 2026
$61.1M
miRNA Regulation of the Mitochondrial GenomeR01HL128485 · NHLBI · WEST VIRGINIA UNIVERSITY · PI HOLLANDER, JOHN M · 2017 to 2019
$1.3M
miRNA Regulation of the Mitochondrial GenomeR56HL128485 · NHLBI · WEST VIRGINIA UNIVERSITY · PI HOLLANDER, JOHN M · 2015 to 2015
$410k
NHLBI NIH HHS R01 HL128485NHLBI NIH HHS R56 HL128485NIGMS NIH HHS P20 GM103434
6 · The paper itself

Abstract

Heart failure (HF) is an end point resulting from a number of disease states. The prognosis for HF patients is poor with survival rates precipitously low. Energy metabolism is centrally linked to the development of HF, and it involves the proteomic remodeling of numerous pathways, many of which are targeted to the mitochondrion. microRNAs (miRNA) are noncoding RNAs that influence posttranscriptional gene regulation. miRNA have garnered considerable attention for their ability to orchestrate changes to the transcriptome, and ultimately the proteome, during HF. Recently, interest in the role played by miRNA in the regulation of energy metabolism at the mitochondrion has emerged. Cardiac proteome remodeling during HF includes axes impacting hypertrophy, oxidative stress, calcium homeostasis, and metabolic fuel transition. Although it is established that the pathological environment of hypoxia and hemodynamic stress significantly contribute to the HF phenotype, it remains unclear as to the mechanistic underpinnings driving proteome remodeling. The aim of this review is to present evidence highlighting the role played by miRNA in these processes as a means for linking pathological stimuli with proteomic alteration. The differential expression of proteins of substrate transport, glycolysis, β-oxidation, ketone metabolism, the citric acid cycle (CAC), and the electron transport chain (ETC) are paralleled by the differential expression of miRNA species that modulate these processes. Identification of miRNAs that translocate to cardiomyocyte mitochondria (miR-181c, miR-378) influencing the expression of the mitochondrial genome-encoded transcripts as well as suggested import modulators are discussed. Current insights, applications, and challenges of miRNA-based therapeutics are also described.

Indexed as

CalciumCardiomegalyEnergy MetabolismHeart FailureHemodynamicsHumansHypoxiaMicroRNAsMitochondria, HeartMyocytes, CardiacOxidative StressProteomeStress, MechanicalCalciumMicroRNAsProteomeheart failuremetabolismmiRNAmitochondria

Identifiers

PMID27742689
PMCPMC5283914
OpenAlexW2529942664

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.