Evidence map›Paper›PMID 24526677›Full record

ReviewCirculation research2014

Matrix revisited: mechanisms linking energy substrate metabolism to the function of the heart.

Andrew N Carley, Heinrich Taegtmeyer, E Douglas Lewandowski

Open access · bronzeAbstract readReview
In one paragraph

Review in Circulation research, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 69 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
69citing papers in PubMed, 1 pooled it
6.4field-weighted citation impact, top 3% 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

69 citing papers in PubMed, 1 synthesis or guideline pooled it, 99 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Article
  4. Article
  5. Review
  6. UCP1-dependent brown adipose activation accelerates cardiac metabolic remodeling and reduces initial hypertrophic and fibrotic responses to pathological stress.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2024
    Article
  7. Article
  8. Article
  9. Article
  10. Metabolic flux in the driver's seat during cardiac health and disease.Journal of molecular and cellular cardiology · 2023
    Review
  11. Review
  12. Article
  13. Review
  14. Unravelling the Interplay between Cardiac Metabolism and Heart Regeneration.International journal of molecular sciences · 2023
    Review
  15. Article
  16. Article
  17. Review
  18. Reactivation of PPARActa pharmaceutica Sinica. B · 2023
    Article
  19. The impact of diet upon mitochondrial physiology (Review).International journal of molecular medicine · 2022
    Review
  20. Article

9 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.

Andrew N CarleyFrom the Center for Cardiovascular Research, University of Illinois at Chicago College of Medicine, Chicago IL (A.N.C., E.D.L.); and Department of Internal Medicine, Division of Cardiology, The University of Texas Medical School at Houston (H.T.).
Heinrich Taegtmeyer
E Douglas Lewandowski
Texas Medical Center · US

Funding

SWITCHING OF METABOLIC GENES IN UNLOADED HEARTR01HL061483 · NHLBI · UNIVERSITY OF TEXAS HLTH SCI CTR HOUSTON · PI TAEGTMEYER, HEINRICH · 1999 to 2021
$6.2M
NHLBI NIH HHS R01 HL061483
6 · The paper itself

Abstract

Metabolic signaling mechanisms are increasingly recognized to mediate the cellular response to alterations in workload demand, as a consequence of physiological and pathophysiological challenges. Thus, an understanding of the metabolic mechanisms coordinating activity in the cytosol with the energy-providing pathways in the mitochondrial matrix becomes critical for deepening our insights into the pathogenic changes that occur in the stressed cardiomyocyte. Processes that exchange both metabolic intermediates and cations between the cytosol and mitochondria enable transduction of dynamic changes in contractile state to the mitochondrial compartment of the cell. Disruption of such metabolic transduction pathways has severe consequences for the energetic support of contractile function in the heart and is implicated in the pathogenesis of heart failure. Deficiencies in metabolic reserve and impaired metabolic transduction in the cardiomyocyte can result from inherent deficiencies in metabolic phenotype or maladaptive changes in metabolic enzyme expression and regulation in the response to pathogenic stress. This review examines both current and emerging concepts of the functional linkage between the cytosol and the mitochondrial matrix with a specific focus on metabolic reserve and energetic efficiency. These principles of exchange and transport mechanisms across the mitochondrial membrane are reviewed for the failing heart from the perspectives of chronic pressure overload and diabetes mellitus.

Indexed as

AnimalsEnergy MetabolismHeartHeart FailureHumansMitochondriaMyocardiumMyocytes, Cardiaccytosoldiabetes mellitusheart failuremetabolic pathwaysmetabolismmitochondriamobilization

Identifiers

PMID24526677
PMCPMC4410983
OpenAlexW2024686537

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.