Evidence map›Paper›PMID 33361348›Full record

ArticleGut2021

RIPK3 acts as a lipid metabolism regulator contributing to inflammation and carcinogenesis in non-alcoholic fatty liver disease.

Marta B Afonso, Pedro M Rodrigues, Miguel Mateus-Pinheiro, André L Simão, Maria M Gaspar, Amine Majdi, Enara Arretxe, Cristina Alonso, Alvaro Santos-Laso, Raul Jimenez-Agüero and 8 more

Open access · hybridAbstract read
In one paragraph

Article in Gut, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 67 papers.

0numbers the graph read from it
0cells of the map it votes in
67citing papers in PubMed
8.4field-weighted citation impact, top 2% 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

67 citing papers in PubMed, 101 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. NovelGut · 2026
    Article
  5. Review
  6. RIPK3 Orchestrates Scar-Associated Macrophage Dysfunction to Drive Pulmonary Fibrosis.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026
    Article
  7. Article
  8. Review
  9. PANoptosis in diabetes: immunometabolic insights and treatments.Apoptosis : an international journal on programmed cell death · 2026
    Review
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  11. Review
  12. Review
  13. Review
  14. Article
  15. Article
  16. Article
  17. Review
  18. Article
  19. Article
  20. Article

7 more citing papers are in PubMed but not listed here.

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

18 authors at 5 institutions in 3 countries.

Marta B AfonsoResearch Institute for Medicines (iMed.ULisboa), Faculty of Pharmacy, Universidade de Lisboa, Lisbon, Portugal.
Pedro M RodriguesResearch Institute for Medicines (iMed.ULisboa), Faculty of Pharmacy, Universidade de Lisboa, Lisbon, Portugal.
Miguel Mateus-PinheiroResearch Institute for Medicines (iMed.ULisboa), Faculty of Pharmacy, Universidade de Lisboa, Lisbon, Portugal.
André L SimãoResearch Institute for Medicines (iMed.ULisboa), Faculty of Pharmacy, Universidade de Lisboa, Lisbon, Portugal.
Maria M GasparResearch Institute for Medicines (iMed.ULisboa), Faculty of Pharmacy, Universidade de Lisboa, Lisbon, Portugal.
Amine MajdiSorbonne Université, Inserm, Centre de Recherche Saint-Antoine (CRSA), Paris, France.
Enara ArretxeOWL Metabolomics, Bizkaia Technology Park, Derio, Spain.
Cristina AlonsoOWL Metabolomics, Bizkaia Technology Park, Derio, Spain.
Alvaro Santos-LasoDepartment of Liver and Gastrointestinal Diseases, Biodonostia Health Research Institute, Donostia University Hospital, University of the Basque Country (UPV/EHU), Ikerbasque, CIBERehd, San Sebastian, Spain.
Raul Jimenez-AgüeroDepartment of Liver and Gastrointestinal Diseases, Biodonostia Health Research Institute, Donostia University Hospital, University of the Basque Country (UPV/EHU), Ikerbasque, CIBERehd, San Sebastian, Spain.
Emma EizaguirreDepartment of Liver and Gastrointestinal Diseases, Biodonostia Health Research Institute, Donostia University Hospital, University of the Basque Country (UPV/EHU), Ikerbasque, CIBERehd, San Sebastian, Spain.
Luis BujandaDepartment of Liver and Gastrointestinal Diseases, Biodonostia Health Research Institute, Donostia University Hospital, University of the Basque Country (UPV/EHU), Ikerbasque, CIBERehd, San Sebastian, Spain.
Maria Jesus ParejaHospital Universitario de Valme, Sevilla, Andalucía, Spain.
Jesus M BanalesDepartment of Liver and Gastrointestinal Diseases, Biodonostia Health Research Institute, Donostia University Hospital, University of the Basque Country (UPV/EHU), Ikerbasque, CIBERehd, San Sebastian, Spain.
Vlad RatziuInstitute of Cardiometabolism and Nutrition (ICAN), Paris, France.
Jeremie GautheronSorbonne Université, Inserm, Centre de Recherche Saint-Antoine (CRSA), Paris, France.
Rui E CastroResearch Institute for Medicines (iMed.ULisboa), Faculty of Pharmacy, Universidade de Lisboa, Lisbon, Portugal.
Cecília M P RodriguesResearch Institute for Medicines (iMed.ULisboa), Faculty of Pharmacy, Universidade de Lisboa, Lisbon, Portugal cmprodrigues@ff.ul.pt.ORCID 0000-0002-4829-754X
University of Lisbon · PTIkerbasque · ESInserm · FREuskadiko Parke Teknologikoa · ESHospital Universitario de Valme · ES

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectiveReceptor-interacting protein kinase 3 (RIPK3) is a key player in necroptosis execution and an emerging metabolic regulator, whose contribution to non-alcoholic fatty liver disease (NAFLD) is controversial. We aimed to clarify the impact of RIPK3 signalling in the pathogenesis of human and experimental NAFLD.

designRIPK3 levels were evaluated in two large independent cohorts of patients with biopsy proven NAFLD diagnosis and correlated with clinical and biochemical parameters. Wild-type (WT) or

resultsRIPK3 increased in patients with non-alcoholic steatohepatitis (NASH) in both cohorts, correlating with hepatic inflammation and fibrosis. Accordingly,

conclusionHepatic RIPK3 correlates with NAFLD severity in humans and mice, playing a key role in managing liver metabolism, damage, inflammation, fibrosis and carcinogenesis. Targeting RIPK3 and its intricate signalling arises as a novel promising approach to treat NASH and arrest disease progression.

Indexed as

AnimalsBiomarkersCarcinogenesisCell Transformation, NeoplasticDisease ProgressionHumansLipid MetabolismLiver CirrhosisLiver NeoplasmsMiceNon-alcoholic Fatty Liver DiseaseProspective StudiesReceptor-Interacting Protein Serine-Threonine KinasesBiomarkersReceptor-Interacting Protein Serine-Threonine KinasesRIPK3 protein, humancell deathchronic liver diseaselipid metabolismmolecular carcinogenesisnonalcoholic steatohepatitis

Identifiers

PMID33361348
PMCPMC8588316
OpenAlexW3117349407

What OpenQuestion holds

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LicenceCC BY-NC
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.