Evidence map›Paper›PMID 25564863›Full record

ArticleBiophysical journal2015

From metabolomics to fluxomics: a computational procedure to translate metabolite profiles into metabolic fluxes.

Sonia Cortassa, Viviane Caceres, Lauren N Bell, Brian O'Rourke, Nazareno Paolocci, Miguel A Aon

Open access · bronzeAbstract read
In one paragraph

Article in Biophysical journal, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.

0numbers the graph read from it
0cells of the map it votes in
40citing papers in PubMed
3.9field-weighted citation impact, top 6% 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

40 citing papers in PubMed, 85 citations in OpenAlex.

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  14. Metabolic signatures of pregnancy-induced cardiac growth.American journal of physiology. Heart and circulatory physiology · 2022
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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

6 authors at 3 institutions in 1 country.

Sonia CortassaDivision of Cardiology, Johns Hopkins University School of Medicine, Baltimore, Maryland.
Viviane CaceresDivision of Cardiology, Johns Hopkins University School of Medicine, Baltimore, Maryland.
Lauren N BellMetabolon, Inc., Durham, North Carolina.
Brian O'RourkeDivision of Cardiology, Johns Hopkins University School of Medicine, Baltimore, Maryland.
Nazareno PaolocciDivision of Cardiology, Johns Hopkins University School of Medicine, Baltimore, Maryland.
Miguel A AonDivision of Cardiology, Johns Hopkins University School of Medicine, Baltimore, Maryland. Electronic address: maon1@jhmi.edu.
Johns Hopkins Medicine · USJohns Hopkins University · USMetabolon (United States) · US

Funding

GSK3b mediates convergence of protection signaling to limit mitochondrial damage ZIAAG000823 · NIA · NATIONAL INSTITUTE ON AGING · PI SOLLOTT, STEVEN · 2009 to 2016
$6.8M
ENERGETIC REGULATION OF CARDIAC ION CHANNELSR37HL054598 · NHLBI · JOHNS HOPKINS UNIVERSITY · PI O'ROURKE, BRIAN · 2005 to 2014
$3.7M
Redox Modification of the Arrhythmic Substrate in Heart FailureR01HL105216 · NHLBI · JOHNS HOPKINS UNIVERSITY · PI O'ROURKE, BRIAN, TRAYANOVA, NATALIA A. · 2011 to 2014
$3.0M
Mechanisms Underlying Mitrochondrial Dysfunction in the Diabetic HeartR01HL091923 · NHLBI · JOHNS HOPKINS UNIVERSITY · PI AKAR, FADI GABRIEL, AON, MIGUEL ANTONIO · 2009 to 2012
$1.9M
Mechanisms of ROS Balance and Cardiac Energy Metabolism in Diabetes MellitusR21HL106054 · NHLBI · JOHNS HOPKINS UNIVERSITY · PI CORTASSA, SONIA DEL CARMEN · 2011 to 2012
$451k
NHLBI NIH HHS R01 HL091923NHLBI NIH HHS R01HL091923-01NHLBI NIH HHS R21 HL106054NHLBI NIH HHS R21HL106054NHLBI NIH HHS R37 HL054598
6 · The paper itself

Abstract

We describe a believed-novel procedure for translating metabolite profiles (metabolome) into the set of metabolic fluxes (fluxome) from which they originated. Methodologically, computational modeling is integrated with an analytical platform comprising linear optimization, continuation and dynamic analyses, and metabolic control. The procedure was tested with metabolite profiles obtained from ex vivo mice Langendorff-heart preparations perfused with glucose. The metabolic profiles were analyzed using a detailed kinetic model of the glucose catabolic pathways including glycolysis, pentose phosphate (PP), glycogenolysis, and polyols to translate the glucose metabolome of the heart into the fluxome. After optimization, the ability of the model to simulate the initial metabolite profile was confirmed, and metabolic fluxes as well as the structure of control and regulation of the glucose catabolic network could be calculated. We show that the step catalyzed by phosphofructokinase together with ATP demand and glycogenolysis exert the highest control on the glycolytic flux. The negative flux control exerted by phosphofructokinase on the PP and polyol pathways revealed that the extent of glycolytic flux directly affects flux redirection through these pathways, i.e., the higher the glycolytic flux the lower the PP and polyols. This believed-novel methodological approach represents a step forward that may help in designing therapeutic strategies targeted to diagnose, prevent, and treat metabolic diseases.

Indexed as

Computer SimulationModels, BiologicalAdenosine TriphosphatasesAnimalsGlucoseGlycogenolysisGlycolysisKineticsLinear ModelsMetabolomeMice, Inbred C57BLMice, TransgenicMyocardiumNADNADPPentose Phosphate PathwayAdenosine TriphosphatasesGlucoseNADNADPPolymerspolyol

Identifiers

PMID25564863
PMCPMC4286601
OpenAlexW2025325354

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.