Evidence map›Paper›PMID 42173920›Full record

ArticleNature communications2026

Blood multiomics reveal a dysregulated lipid mediator-mitochondrial network associated with the outcome of advanced cirrhosis.

Cristina López-Vicario, Ferran Aguilar, Fleur Chapus, Carlos de la Peña-Ramirez, François Fenaille, Florence Castelli, Marta Duran-Güell, Bryan J Contreras, Berta Romero-Grimaldo, María Belén Sánchez-Rodríguez and 19 more

Abstract read
In one paragraph

Article in Nature communications, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

29 authors.

Cristina López-Vicario *Biochemistry and Molecular Genetics Service, Hospital Clínic-IDIBAPS, Barcelona, Spain. clopezv@recerca.clinic.cat.ORCID http://orcid.org/0000-0002-6609-8501
Ferran Aguilar *European Foundation for the Study of Chronic Liver Failure (EF CLIF) and Grifols Chair, Barcelona, Spain.
Fleur Chapus *Biochemistry and Molecular Genetics Service, Hospital Clínic-IDIBAPS, Barcelona, Spain.
Carlos de la Peña-RamirezEuropean Foundation for the Study of Chronic Liver Failure (EF CLIF) and Grifols Chair, Barcelona, Spain.
François FenailleUniversité Paris-Saclay, CEA, INRAE, Département Médicaments et Technologies pour la Santé, MetaboHUB, Gif-sur-Yvette, France.ORCID http://orcid.org/0000-0001-6787-4149
Florence CastelliUniversité Paris-Saclay, CEA, INRAE, Département Médicaments et Technologies pour la Santé, MetaboHUB, Gif-sur-Yvette, France.
Marta Duran-GüellBiochemistry and Molecular Genetics Service, Hospital Clínic-IDIBAPS, Barcelona, Spain.
Bryan J ContrerasBiochemistry and Molecular Genetics Service, Hospital Clínic-IDIBAPS, Barcelona, Spain.
Berta Romero-GrimaldoBiochemistry and Molecular Genetics Service, Hospital Clínic-IDIBAPS, Barcelona, Spain.
María Belén Sánchez-RodríguezBiochemistry and Molecular Genetics Service, Hospital Clínic-IDIBAPS, Barcelona, Spain.
Laura Valls-RocaInherited Metabolic Diseases and Muscular Disorders Research Group, Cellex-IDIBAPS, Faculty of Medicine and Health Sciences-University of Barcelona, Internal Medicine Department-Hospital Clínic, Barcelona, Spain.
Glòria GarrabouInherited Metabolic Diseases and Muscular Disorders Research Group, Cellex-IDIBAPS, Faculty of Medicine and Health Sciences-University of Barcelona, Internal Medicine Department-Hospital Clínic, Barcelona, Spain.
Sara Palomino-EcheverriaTranslational Bioinformatics Unit, Navarrabiomed, Fundacion Miguel Servet, Universidad Publica de Navarra (UPNA), IdiSNA, Pamplona, Spain.
Estefania HuergoTranslational Bioinformatics Unit, Navarrabiomed, Fundacion Miguel Servet, Universidad Publica de Navarra (UPNA), IdiSNA, Pamplona, Spain.
Cristina Sanchez-GarridoEuropean Foundation for the Study of Chronic Liver Failure (EF CLIF) and Grifols Chair, Barcelona, Spain.
Wim LalemanUniversity of Leuven, Leuven, Belgium.
David Gómez-CabreroTranslational Bioinformatics Unit, Navarrabiomed, Fundacion Miguel Servet, Universidad Publica de Navarra (UPNA), IdiSNA, Pamplona, Spain.ORCID http://orcid.org/0000-0003-4186-3788
Alberto Queiroz FariasDepartment of Gastroenterology, Hospital das Clínicas, University of São Paulo School of Medicine, São Paulo, Brazil.
Sebastián MarcianoLiver Unit and Department of Research, Hospital Italiano de Buenos Aires, Buenos Aires, Argentina.
Paolo CaraceniDepartment of Medical and Surgical Sciences, University of Bologna, Bologna, Italy.
Jonel TrebickaEuropean Foundation for the Study of Chronic Liver Failure (EF CLIF) and Grifols Chair, Barcelona, Spain.ORCID http://orcid.org/0000-0002-7028-3881
Javier FernándezEuropean Foundation for the Study of Chronic Liver Failure (EF CLIF) and Grifols Chair, Barcelona, Spain.
Christophe JunotUniversité Paris-Saclay, CEA, INRAE, Département Médicaments et Technologies pour la Santé, MetaboHUB, Gif-sur-Yvette, France.
Esther TitosBiochemistry and Molecular Genetics Service, Hospital Clínic-IDIBAPS, Barcelona, Spain.ORCID http://orcid.org/0000-0002-2543-2243
Richard MoreauEuropean Foundation for the Study of Chronic Liver Failure (EF CLIF) and Grifols Chair, Barcelona, Spain.ORCID http://orcid.org/0000-0003-0862-403X
Vicente ArroyoEuropean Foundation for the Study of Chronic Liver Failure (EF CLIF) and Grifols Chair, Barcelona, Spain.
Pierre-Emmanuel RautouUniversité Paris-Cité, Inserm, Centre de recherche sur l'inflammation, UMR, Paris, France.ORCID http://orcid.org/0000-0001-9567-1859
Joan ClàriaBiochemistry and Molecular Genetics Service, Hospital Clínic-IDIBAPS, Barcelona, Spain. jclaria@clinic.cat.ORCID http://orcid.org/0000-0003-4333-7749
DECISION Consortium

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The mechanisms driving the progression from acutely decompensated (AD) cirrhosis to acute-on-chronic liver failure (ACLF), a high mortality condition, remain poorly understood. In this study, we integrate multiomics and clinical data from 766 AD patients to construct multiscale, multifactorial response networks associated with two major outcomes: ACLF development and death. Among 291 features, 22 are linked to ACLF development and 16 to mortality. These features constitute a network connecting mitochondrial dysfunction with the accumulation of the lipid mediator 20-hydroxyeicosatetraenoic acid (20-HETE). In vitro validation of this network in human peripheral leukocytes shows that 20-HETE induces mitochondrial oxidative stress and impairs mitochondrial respiration via a GPR75-Akt signaling pathway. Network features also act as early predictors of AD outcomes, a finding validated in an independent cohort of 580 patients. Here, we show a strong link between dysregulated immunomodulatory lipid mediators and mitochondrial dysfunction driving ACLF development and mortality risk in advanced cirrhosis.

Indexed as

Acute-On-Chronic Liver FailureLiver CirrhosisMitochondriaDisease ProgressionFemaleHumansHydroxyeicosatetraenoic AcidsLipid MetabolismMaleMiddle AgedMultiomicsOxidative StressReceptors, G-Protein-CoupledSignal TransductionHydroxyeicosatetraenoic AcidsReceptors, G-Protein-Coupled

Identifiers

PMID42173920
PMCPMC13385380

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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.