Evidence map›Paper›PMID 39570879›Full record

ReviewCardiovascular research2024

Anaplerotic filling in heart failure: a review of mechanism and potential therapeutics.

Karm A Alhasan, Melissa A King, Badal S B Pattar, Ian A Lewis, Gary D Lopaschuk, Steven C Greenway

Abstract readReview
In one paragraph

Review in Cardiovascular research, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
–field-weighted citation impact
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

7 citing papers in PubMed.

  1. Article
  2. Nuclear m6A Methylase METTL3 Drives Production of ITGβ4E to Exacerbate Heart Failure via SRSF3-Mediated Alternative Splicing of ITGβ4.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026
    Article
  3. Review
  4. Article
  5. Molecular and cellular mechanisms of pentadecanoic acid.World journal of biological chemistry · 2025
    Review
  6. Article
  7. 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

6 authors.

Karm A AlhasanDepartment of Cardiac Sciences and Libin Cardiovascular Institute, Cumming School of Medicine, University of Calgary, Calgary, AB, Canada T2N 4N1.ORCID 0009-0003-0563-8804
Melissa A KingDepartment of Cardiac Sciences and Libin Cardiovascular Institute, Cumming School of Medicine, University of Calgary, Calgary, AB, Canada T2N 4N1.
Badal S B PattarDepartment of Cardiac Sciences and Libin Cardiovascular Institute, Cumming School of Medicine, University of Calgary, Calgary, AB, Canada T2N 4N1.
Ian A LewisAlberta Centre for Advanced Diagnostics, Department of Biological Sciences, University of Calgary, Calgary, AB, Canada T2N 1N4.
Gary D LopaschukCardiovascular Research Centre, University of Alberta, Edmonton, AB, Canada T6G 2S2.
Steven C GreenwayDepartment of Cardiac Sciences and Libin Cardiovascular Institute, Cumming School of Medicine, University of Calgary, Calgary, AB, Canada T2N 4N1.ORCID 0000-0002-6981-1720

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Heart failure (HF) is a complex syndrome and a leading cause of mortality worldwide. While current medical treatment is based on known pathophysiology and is effective for many patients, the underlying cellular mechanisms are poorly understood. Energy deficiency is a characteristic of HF, marked by complex alterations in metabolism. Within the tricarboxylic acid cycle, anaplerosis emerges as an essential metabolic process responsible for replenishing lost intermediates, thereby playing a crucial role in sustaining energy metabolism and consequently cardiac function. Alterations in cardiac anaplerosis are commonly observed in HF, demonstrating potential for therapeutic intervention. This review discusses recent advances in understanding the anaplerotic adaptations that occur in HF. We also explore therapeutics that can directly modulate anaplerosis or are likely to confer cardioprotective effects through anaplerosis, which could potentially be implemented to rescue the failing heart.

Indexed as

Citric Acid CycleEnergy MetabolismHeart FailureAnimalsHumansMyocardiumVentricular Function, LeftAnaplerosisCardiac metabolismCardiovascular diseaseHeart failureMitochondria

Identifiers

PMID39570879
PMCPMC11687400

What OpenQuestion holds

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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.