Evidence map›Paper›PMID 38216754›Full record

ArticleMolecular systems biology2024

Basal MET phosphorylation is an indicator of hepatocyte dysregulation in liver disease.

Sebastian Burbano de Lara, Svenja Kemmer, Ina Biermayer, Svenja Feiler, Artyom Vlasov, Lorenza A D'Alessandro, Barbara Helm, Christina Mölders, Yannik Dieter, Ahmed Ghallab and 11 more

Open access · goldAbstract read
In one paragraph

Article in Molecular systems biology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
3.3field-weighted citation impact, top 8% 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

6 citing papers in PubMed, 9 citations in OpenAlex.

  1. Article
  2. BioModels' model of the year 2024.Frontiers in systems biology · 2026
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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

21 authors at 6 institutions in 3 countries.

Sebastian Burbano de Lara *Division Systems Biology of Signal Transduction, German Cancer Research Center (DKFZ), Heidelberg, Germany.ORCID http://orcid.org/0000-0002-5364-2686
Svenja Kemmer *Liver Systems Medicine against Cancer (LiSyM-Krebs), Heidelberg, Germany.ORCID http://orcid.org/0000-0001-7708-0545
Ina Biermayer *Division Systems Biology of Signal Transduction, German Cancer Research Center (DKFZ), Heidelberg, Germany.
Svenja FeilerDivision Systems Biology of Signal Transduction, German Cancer Research Center (DKFZ), Heidelberg, Germany.
Artyom VlasovDivision Systems Biology of Signal Transduction, German Cancer Research Center (DKFZ), Heidelberg, Germany.
Lorenza A D'AlessandroDivision Systems Biology of Signal Transduction, German Cancer Research Center (DKFZ), Heidelberg, Germany.
Barbara HelmDivision Systems Biology of Signal Transduction, German Cancer Research Center (DKFZ), Heidelberg, Germany.
Christina MöldersDivision Systems Biology of Signal Transduction, German Cancer Research Center (DKFZ), Heidelberg, Germany.
Yannik DieterDivision Systems Biology of Signal Transduction, German Cancer Research Center (DKFZ), Heidelberg, Germany.ORCID http://orcid.org/0009-0004-2599-7879
Ahmed GhallabSystems Toxicology, Leibniz Research Center for Working Environment and Human Factors, Technical University Dortmund, Dortmund, Germany.ORCID http://orcid.org/0000-0003-0695-3403
Jan G HengstlerLiver Systems Medicine against Cancer (LiSyM-Krebs), Heidelberg, Germany.
Christiane KörnerLiver Systems Medicine against Cancer (LiSyM-Krebs), Heidelberg, Germany.ORCID http://orcid.org/0000-0001-8753-8441
Madlen Matz-SojaLiver Systems Medicine against Cancer (LiSyM-Krebs), Heidelberg, Germany.
Christina GötzLiver Systems Medicine against Cancer (LiSyM-Krebs), Heidelberg, Germany.ORCID http://orcid.org/0000-0002-8060-1599
Georg DammLiver Systems Medicine against Cancer (LiSyM-Krebs), Heidelberg, Germany.
Katrin HoffmannLiver Systems Medicine against Cancer (LiSyM-Krebs), Heidelberg, Germany.
Daniel SeehoferLiver Systems Medicine against Cancer (LiSyM-Krebs), Heidelberg, Germany.
Thomas BergLiver Systems Medicine against Cancer (LiSyM-Krebs), Heidelberg, Germany.
Marcel SchillingDivision Systems Biology of Signal Transduction, German Cancer Research Center (DKFZ), Heidelberg, Germany. m.schilling@dkfz.de.ORCID http://orcid.org/0000-0002-9517-5166
Jens TimmerLiver Systems Medicine against Cancer (LiSyM-Krebs), Heidelberg, Germany. jeti@fdm.uni-freiburg.ORCID http://orcid.org/0000-0003-4517-1383
Ursula KlingmüllerDivision Systems Biology of Signal Transduction, German Cancer Research Center (DKFZ), Heidelberg, Germany. u.klingmueller@dkfz.de.ORCID http://orcid.org/0000-0001-9845-3099
German Cancer Research Center · DELeague Against Cancer · USUniversity of Freiburg · DEHeidelberg University · DESouth Valley University · EGTU Dortmund University · DE

Funding

Baden-Württemberg bwHPCBundesministerium für Bildung und Forschung (BMBF) 031L0042Bundesministerium für Bildung und Forschung (BMBF) 031L0045Bundesministerium für Bildung und Forschung (BMBF) 031L0048Bundesministerium für Bildung und Forschung (BMBF) 031L0049Bundesministerium für Bildung und Forschung (BMBF) 031L0052Bundesministerium für Bildung und Forschung (BMBF) 031L0212BBundesministerium für Bildung und Forschung (BMBF) 031L0256ABundesministerium für Bildung und Forschung (BMBF) 031L0256BBundesministerium für Bildung und Forschung (BMBF) 031L0256CBundesministerium für Bildung und Forschung (BMBF) 031L0256GBundesministerium für Bildung und Forschung (BMBF) 031L0257CBundesministerium für Bildung und Forschung (BMBF) 031L0257DBundesministerium für Bildung und Forschung (BMBF) 031L0257KBundesministerium für Bildung und Forschung (BMBF) 031L0258EBundesministerium für Bildung und Forschung (BMBF) 82DZL004A4Deutsche Forschungsgemeinschaft (DFG) 457840828University of Freiburg Open Access Publication Fund
6 · The paper itself

Abstract

Chronic liver diseases are worldwide on the rise. Due to the rapidly increasing incidence, in particular in Western countries, metabolic dysfunction-associated steatotic liver disease (MASLD) is gaining importance as the disease can develop into hepatocellular carcinoma. Lipid accumulation in hepatocytes has been identified as the characteristic structural change in MASLD development, but molecular mechanisms responsible for disease progression remained unresolved. Here, we uncover in primary hepatocytes from a preclinical model fed with a Western diet (WD) an increased basal MET phosphorylation and a strong downregulation of the PI3K-AKT pathway. Dynamic pathway modeling of hepatocyte growth factor (HGF) signal transduction combined with global proteomics identifies that an elevated basal MET phosphorylation rate is the main driver of altered signaling leading to increased proliferation of WD-hepatocytes. Model-adaptation to patient-derived hepatocytes reveal patient-specific variability in basal MET phosphorylation, which correlates with patient outcome after liver surgery. Thus, dysregulated basal MET phosphorylation could be an indicator for the health status of the liver and thereby inform on the risk of a patient to suffer from liver failure after surgery.

Indexed as

Carcinoma, HepatocellularFatty LiverLiver NeoplasmsHepatocyte Growth FactorHepatocytesHumansPhosphatidylinositol 3-KinasesPhosphorylationHepatocyte Growth FactorPhosphatidylinositol 3-KinasesDynamic Pathway ModelingFatty Liver DiseaseHepatocyte DysregulationHGF Signal TransductionWestern Diet

Identifiers

PMID38216754
PMCPMC10912216
OpenAlexW4390815751

What Socratic 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 Socratic graph.