Evidence map›Paper›PMID 29558460›Full record

ReviewInternational journal of molecular sciences2018

p53 as a Dichotomous Regulator of Liver Disease: The Dose Makes the Medicine.

Jelena Krstic, Markus Galhuber, Tim J Schulz, Michael Schupp, Andreas Prokesch

Open access · goldAbstract readReview
In one paragraph

Review in International journal of molecular sciences, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed
3.9field-weighted citation impact, top 6% 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

33 citing papers in PubMed, 59 citations in OpenAlex.

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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

5 authors at 3 institutions in 2 countries.

Jelena KrsticGottfried Schatz Research Center for Cell Signaling, Metabolism & Aging, Medical University of Graz, 8010 Graz, Austria. jelena.krstic@medunigraz.at.
Markus GalhuberGottfried Schatz Research Center for Cell Signaling, Metabolism & Aging, Medical University of Graz, 8010 Graz, Austria. markus.galhuber@medunigraz.at.
Tim J SchulzDepartment of Adipocyte Development and Nutrition, German Institute of Human Nutrition, Potsdam-Rehhbrücke, 14558 Nuthetal, Germany. tim.schulz@dife.de.
Michael SchuppCharité-Universitätsmedizin Berlin, Corporate Member of Freie Universität Berlin, Humboldt-Universität zu Berlin, and Berlin Institute of Health, Institute of Pharmacology, Center for Cardiovascular Research, 10117 Berlin, Germany. michael.schupp@charite.de.
Andreas ProkeschGottfried Schatz Research Center for Cell Signaling, Metabolism & Aging, Medical University of Graz, 8010 Graz, Austria. andreas.prokesch@medunigraz.at.
Medical University of Graz · ATHumboldt-Universität zu Berlin · DEUniversity of Potsdam · DE

Funding

Austrian Science Fund FWF I 3165Austrian Science Fund FWF P 29328
6 · The paper itself

Abstract

Lifestyle-related disorders, such as the metabolic syndrome, have become a primary risk factor for the development of liver pathologies that can progress from hepatic steatosis, hepatic insulin resistance, steatohepatitis, fibrosis and cirrhosis, to the most severe condition of hepatocellular carcinoma (HCC). While the prevalence of liver pathologies is steadily increasing in modern societies, there are currently no approved drugs other than chemotherapeutic intervention in late stage HCC. Hence, there is a pressing need to identify and investigate causative molecular pathways that can yield new therapeutic avenues. The transcription factor p53 is well established as a tumor suppressor and has recently been described as a central metabolic player both in physiological and pathological settings. Given that liver is a dynamic tissue with direct exposition to ingested nutrients, hepatic p53, by integrating cellular stress response, metabolism and cell cycle regulation, has emerged as an important regulator of liver homeostasis and dysfunction. The underlying evidence is reviewed herein, with a focus on clinical data and animal studies that highlight a direct influence of p53 activity on different stages of liver diseases. Based on current literature showing that activation of p53 signaling can either attenuate or fuel liver disease, we herein discuss the hypothesis that, while hyper-activation or loss of function can cause disease, moderate induction of hepatic p53 within physiological margins could be beneficial in the prevention and treatment of liver pathologies. Hence, stimuli that lead to a moderate and temporary p53 activation could present new therapeutic approaches through several entry points in the cascade from hepatic steatosis to HCC.

Indexed as

AnimalsHumansLiver DiseasesTumor Suppressor Protein p53Tumor Suppressor Protein p53hepatocellular carcinomainsulin resistanceliver diseaseliver regenerationmouse modelsnon-alcoholic fatty liver diseasenon-alcoholic steatohepatitisp53

Identifiers

PMID29558460
PMCPMC5877782
OpenAlexW2792709052

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.