Evidence map›Paper›PMID 28196650›Full record

ArticleFree radical biology & medicine2017

Protective role of p53 in acetaminophen hepatotoxicity.

Yazhen Huo, Shutao Yin, Mingzhu Yan, Sanda Win, Tin Aung Than, Mariam Aghajan, Hongbo Hu, Neil Kaplowitz

Abstract read
In one paragraph

Article in Free radical biology & medicine, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.

0numbers the graph read from it
0cells of the map it votes in
34citing papers in PubMed
6.3field-weighted citation impact, top 4% 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

34 citing papers in PubMed, 46 citations in OpenAlex.

  1. On the Edge of Benefit and Harm: Reactive Oxygen Species in Cancer.International journal of molecular sciences · 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

8 authors at 3 institutions in 2 countries.

Yazhen HuoBeijing Advanced Innovation Center for Food Nutrition and Human Health, College of Food Science and Nutritional Engineering, China Agricultural University, Beijing 100083, China.
Shutao YinBeijing Advanced Innovation Center for Food Nutrition and Human Health, College of Food Science and Nutritional Engineering, China Agricultural University, Beijing 100083, China.
Mingzhu YanBeijing Advanced Innovation Center for Food Nutrition and Human Health, College of Food Science and Nutritional Engineering, China Agricultural University, Beijing 100083, China.
Sanda WinUSC Research Center for Liver Disease, Keck School of Medicine of USC, Los Angeles, CA 90033, United States.
Tin Aung ThanUSC Research Center for Liver Disease, Keck School of Medicine of USC, Los Angeles, CA 90033, United States.
Mariam AghajanIONIS Pharmaceuticals, Inc., Carlsbad, CA 92010, United States.
Hongbo HuBeijing Advanced Innovation Center for Food Nutrition and Human Health, College of Food Science and Nutritional Engineering, China Agricultural University, Beijing 100083, China. Electronic address: hongbo@cau.edu.cn.
Neil KaplowitzUSC Research Center for Liver Disease, Keck School of Medicine of USC, Los Angeles, CA 90033, United States. Electronic address: kaplowit@usc.edu.
China Agricultural University · CNKeck Hospital of USC · USIonis Pharmaceuticals (United States) · US

Funding

USC RESEARCH CENTER FOR LIVER DISEASES: PILOT PROGRAMSP30DK048522 · NIDDK · UNIVERSITY OF SOUTHERN CALIFORNIA · PI OOKHTENS, MURAD · 1995 to 2020
$21.8M
Role of Glutathione Redox Status in HepatotoxicityR01DK067215 · NIDDK · UNIVERSITY OF SOUTHERN CALIFORNIA · PI KAPLOWITZ, NEIL · 2005 to 2019
$5.6M
NIDDK NIH HHS P30 DK048522NIDDK NIH HHS R01 DK067215
6 · The paper itself

Abstract

p53 is a tumor suppressor with a pro-death role in many conditions. However, in some contexts, evidence supports a pro-survival function. p53 has been shown to be activated in acetaminophen (APAP) toxicity but the impact of this on toxicity is uncertain. In the present study, we have found that p53 plays a protective role in APAP-induced liver injury. We inhibited p53 using three different approaches in mice, pifithrin-α (PFTα), knockdown of p53 expression with antisense oligonucleotide, and p53 knockout. Mice were treated with APAP (300mg/kg) i.p. and after 24h in all three conditions, the liver injury was more severe as reflected in higher ALT levels and great area of necrosis in histology of the liver. Conversely, a p53 activator, nutlin-3a, decreased the liver injury induced by APAP. In the p53 inhibition models, enhanced sustained JNK activation was seen in the early time course, while the JNK was suppressed with the p53 activator. In conclusion, p53 plays a novel protective role in APAP induced liver injury through inhibiting the activation of JNK, a key mediator in APAP-induced oxidative stress.

Indexed as

AcetaminophenAnimalsBenzothiazolesChemical and Drug Induced Liver InjuryGene Knockdown TechniquesGene Knockout TechniquesHepatocytesHumansImidazolesLiverMAP Kinase Kinase 4MiceOligonucleotides, AntisensePiperazinesSignal TransductionTolueneAcetaminophenBenzothiazolesImidazolesMAP Kinase Kinase 4nutlin 3Oligonucleotides, AntisensepifithrinPiperazinesTolueneTumor Suppressor Protein p53AcetaminophenJNKLiver injuryP53

Identifiers

PMID28196650
PMCPMC5396540
OpenAlexW2587531375

What OpenQuestion holds

Textmetadata
LicenceTDM
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.