Evidence map›Paper›PMID 32201876›Full record

ReviewBriefings in bioinformatics2021

Addressing the heterogeneity in liver diseases using biological networks.

Simon Lam, Stephen Doran, Hatice Hilal Yuksel, Ozlem Altay, Hasan Turkez, Jens Nielsen, Jan Boren, Mathias Uhlen, Adil Mardinoglu

Abstract readReview
In one paragraph

Review in Briefings in bioinformatics, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing 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

4 citing papers in PubMed.

  1. Article
  2. Article
  3. Article
  4. 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

9 authors.

Simon LamCentre for Host-Microbiome Interactions, Faculty of Dentistry, Oral & Craniofacial Sciences, King's College London, London, SE1 9RT, United Kingdom; Science for Life Laboratory, KTH - Royal Institute of Technology, Stockholm, SE-17121, Sweden.
Stephen DoranCentre for Host-Microbiome Interactions, Faculty of Dentistry, Oral & Craniofacial Sciences, King's College London, London, SE1 9RT, United Kingdom; Science for Life Laboratory, KTH - Royal Institute of Technology, Stockholm, SE-17121, Sweden.
Hatice Hilal YukselCentre for Host-Microbiome Interactions, Faculty of Dentistry, Oral & Craniofacial Sciences, King's College London, London, SE1 9RT, United Kingdom; Science for Life Laboratory, KTH - Royal Institute of Technology, Stockholm, SE-17121, Sweden.
Ozlem AltayCentre for Host-Microbiome Interactions, Faculty of Dentistry, Oral & Craniofacial Sciences, King's College London, London, SE1 9RT, United Kingdom; Science for Life Laboratory, KTH - Royal Institute of Technology, Stockholm, SE-17121, Sweden.
Hasan TurkezCentre for Host-Microbiome Interactions, Faculty of Dentistry, Oral & Craniofacial Sciences, King's College London, London, SE1 9RT, United Kingdom; Science for Life Laboratory, KTH - Royal Institute of Technology, Stockholm, SE-17121, Sweden.
Jens NielsenCentre for Host-Microbiome Interactions, Faculty of Dentistry, Oral & Craniofacial Sciences, King's College London, London, SE1 9RT, United Kingdom; Science for Life Laboratory, KTH - Royal Institute of Technology, Stockholm, SE-17121, Sweden.
Jan BorenCentre for Host-Microbiome Interactions, Faculty of Dentistry, Oral & Craniofacial Sciences, King's College London, London, SE1 9RT, United Kingdom; Science for Life Laboratory, KTH - Royal Institute of Technology, Stockholm, SE-17121, Sweden.
Mathias UhlenCentre for Host-Microbiome Interactions, Faculty of Dentistry, Oral & Craniofacial Sciences, King's College London, London, SE1 9RT, United Kingdom; Science for Life Laboratory, KTH - Royal Institute of Technology, Stockholm, SE-17121, Sweden.
Adil MardinogluCentre for Host-Microbiome Interactions, Faculty of Dentistry, Oral & Craniofacial Sciences, King's College London, London, SE1 9RT, United Kingdom; Science for Life Laboratory, KTH - Royal Institute of Technology, Stockholm, SE-17121, Sweden.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The abnormalities in human metabolism have been implicated in the progression of several complex human diseases, including certain cancers. Hence, deciphering the underlying molecular mechanisms associated with metabolic reprogramming in a disease state can greatly assist in elucidating the disease aetiology. An invaluable tool for establishing connections between global metabolic reprogramming and disease development is the genome-scale metabolic model (GEM). Here, we review recent work on the reconstruction of cell/tissue-type and cancer-specific GEMs and their use in identifying metabolic changes occurring in response to liver disease development, stratification of the heterogeneous disease population and discovery of novel drug targets and biomarkers. We also discuss how GEMs can be integrated with other biological networks for generating more comprehensive cell/tissue models. In addition, we review the various biological network analyses that have been employed for the development of efficient treatment strategies. Finally, we present three case studies in which independent studies converged on conclusions underlying liver disease.

Indexed as

Computational BiologyGene Expression ProfilingHumansLiver DiseasesLiver NeoplasmsPyruvate KinaseSurvival RateSystems BiologyPyruvate KinaseComputational biologyGenome-scale metabolic modelIntegrated networkLiver metabolismOmics integrationSystems biology

Identifiers

PMID32201876
PMCPMC7986590

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.