Evidence map›Paper›PMID 27387528›Full record

ArticleIntensive care medicine experimental2016

Transcriptional reprogramming of metabolic pathways in critically ill patients.

Marek Nalos, Grant Parnell, Robert Robergs, David Booth, Anthony S McLean, Benjamin M Tang

Open access · goldAbstract read
In one paragraph

Article in Intensive care medicine experimental, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
1.4field-weighted citation impact, top 20% 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

18 citing papers in PubMed, 37 citations in OpenAlex.

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  6. High-resolution plasma metabolomics and thiamine status in critically Ill adult patients.Metabolomics : Official journal of the Metabolomic Society · 2024
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  17. Lactate and Immunosuppression in Sepsis.Shock (Augusta, Ga.) · 2018
    Review
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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.

Marek NalosNepean Genomic Research Group, Department of Intensive Care Medicine, Nepean Clinical School, University of Sydney, Sydney, Australia. mareknalos@gmail.com.
Grant ParnellNepean Genomic Research Group, Department of Intensive Care Medicine, Nepean Clinical School, University of Sydney, Sydney, Australia.
Robert RobergsQueensland University of Technology, Brisbane, Queensland, Australia.
David BoothCentre for Immunology and Allergy Research, Westmead Millennium Institute, Sydney, Australia.
Anthony S McLeanNepean Genomic Research Group, Department of Intensive Care Medicine, Nepean Clinical School, University of Sydney, Sydney, Australia.
Benjamin M TangNepean Genomic Research Group, Department of Intensive Care Medicine, Nepean Clinical School, University of Sydney, Sydney, Australia.
University of Sydney · AUNepean Hospital · AUQueensland University of Technology · AU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundCritical illness causes a shift away from mitochondrial metabolism towards a greater dependence on glycolysis. This metabolic shift is thought to be associated with lactic acidosis, organ dysfunction and poor clinical outcomes. The current paradigm is that low oxygen supply causes regional hypoxia, which in turn drives such a metabolic shift. In this study, we evaluated whether the shift towards glycolysis can also occur in cells where oxygen supply is plentiful.

methodsWe used circulating blood cells from non-hypoxic critically ill patients (n = 47) as a model to study cellular metabolism in a normal oxygen milieu. We measured the transcriptomic profiles of canonical metabolic pathways in these cells and compared them to cells obtained from healthy controls (n = 18).

resultsTranscriptomic profiling revealed a significant reprogramming of metabolic pathways during critical illness. In well-oxygenated cells, there was a reduced expression of tricarboxylic acid cycle genes and genes associated with pyruvate entry into the mitochondria suggesting decreased mitochondrial oxidation. In contrast, glycolysis was accelerated, as reflected by an up-regulation of genes coding for enzymes of early and late glycolytic pathway that were associated with increased lactate production. The pentose phosphate pathway genes for NADPH production were also up-regulated suggesting enhanced antioxidant production during increased oxidative stress.

conclusionsContrary to the established paradigm, aerobic glycolysis does occur in non-hypoxic cells during critical illness and its occurrence may represent an adaptive strategy common to cells under increased oxidative stress. Further study of this previously under-recognized metabolic phenomenon might identify novel drug target for antioxidant therapy.

Indexed as

Critical illnessGene expressionMetabolismOxidation-reduction

Identifiers

PMID27387528
PMCPMC4936987
OpenAlexW2464948069

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.