Evidence map›Paper›PMID 33588102›Full record

ReviewMolecular metabolism2021

Stress kinases in the development of liver steatosis and hepatocellular carcinoma.

Beatriz Cicuéndez, Irene Ruiz-Garrido, Alfonso Mora, Guadalupe Sabio

Open access · goldAbstract readReview
In one paragraph

Review in Molecular metabolism, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
5.7field-weighted citation impact, top 3% 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

22 citing papers in PubMed, 46 citations in OpenAlex.

  1. The E3 Ligase RNF8 Promotes Ubiquitination and Degradation of ChREBPα During Liver Stress Response.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026
    Article
  2. Attack of the kinases: JNK signaling in metabolism.American journal of physiology. Regulatory, integrative and comparative physiology · 2026
    Review
  3. Article
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  8. Microcystin-LR activates serine/threonine kinases and alters the phosphoproteome in human HepaRG cells.Toxicon : official journal of the International Society on Toxinology · 2024
    Article
  9. Review
  10. Article
  11. Article
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  13. Pirfenidone ameliorates liver steatosis by targeting the STAT3-SCD1 axis.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2023
    Article
  14. Article
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  16. Elucidation of Natural Components ofMolecules (Basel, Switzerland) · 2023
    Article
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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

4 authors at 1 institution in 1 country.

Beatriz CicuéndezCentro Nacional de Investigaciones Cardiovasculares (CNIC), 28029 Madrid, Spain.
Irene Ruiz-GarridoCentro Nacional de Investigaciones Cardiovasculares (CNIC), 28029 Madrid, Spain.
Alfonso MoraCentro Nacional de Investigaciones Cardiovasculares (CNIC), 28029 Madrid, Spain. Electronic address: amora@cnic.es.
Guadalupe SabioCentro Nacional de Investigaciones Cardiovasculares (CNIC), 28029 Madrid, Spain. Electronic address: gsabio@cnic.es.
Spanish National Centre for Cardiovascular Research · ES

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Non-alcoholic fatty liver disease (NAFLD) is an important component of metabolic syndrome and one of the most prevalent liver diseases worldwide. This disorder is closely linked to hepatic insulin resistance, lipotoxicity, and inflammation. Although the mechanisms that cause steatosis and chronic liver injury in NAFLD remain unclear, a key component of this process is the activation of stress-activated kinases (SAPKs), including p38 and JNK in the liver and immune system. This review summarizes findings which indicate that the dysregulation of stress kinases plays a fundamental role in the development of steatosis and are important players in inducing liver fibrosis. To avoid the development of steatohepatitis and liver cancer, SAPK activity must be tightly regulated not only in the hepatocytes but also in other tissues, including cells of the immune system. Possible cellular mechanisms of SAPK actions are discussed.

Indexed as

MAP Kinase Signaling SystemAnimalsAutophagyCarcinoma, HepatocellularDisease Models, AnimalHumansInsulin ResistanceJNK Mitogen-Activated Protein KinasesLiverLiver NeoplasmsNon-alcoholic Fatty Liver Diseasep38 Mitogen-Activated Protein KinasesProtective AgentsJNK Mitogen-Activated Protein Kinasesp38 Mitogen-Activated Protein KinasesProtective AgentsHepatocarcinomaJNKMetabolismp38SAPKSteatosis

Identifiers

PMID33588102
PMCPMC8324677
OpenAlexW3130261553

What Socratic holds

Textmetadata
LicenceCC BY-NC-ND
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.