Evidence map›Paper›PMID 30021675›Full record

ArticleBMB reports2019

Inactivation of Sirtuin2 protects mice from acetaminophen-induced liver injury: possible involvement of ER stress and S6K1 activation.

Da Hyun Lee, Buhyun Lee, Jeong Su Park, Yu Seol Lee, Jin Hee Kim, Yejin Cho, Yoonjung Jo, Hyun-Seok Kim, Yong-Ho Lee, Ki Taek Nam and 1 more

Open access · goldAbstract read
In one paragraph

Article in BMB reports, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
2.3field-weighted citation impact, top 13% 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

10 citing papers in PubMed, 17 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Acetaminophen Hepatotoxicity.Seminars in liver disease · 2019
    Article
  10. Article
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

11 authors at 3 institutions in 2 countries.

Da Hyun LeeBrain Korea 21 PLUS Project for Medical Science, Yonsei University, Seoul 03722; Severance Biomedical Science Institute, Yonsei Biomedical Research Institute, Yonsei University College of Medicine, Seoul 03722, Korea.
Buhyun LeeBrain Korea 21 PLUS Project for Medical Science, Yonsei University, Seoul 03722; Severance Biomedical Science Institute, Yonsei Biomedical Research Institute, Yonsei University College of Medicine, Seoul 03722, Korea.
Jeong Su ParkSeverance Biomedical Science Institute, Yonsei Biomedical Research Institute, Yonsei University College of Medicine, Seoul 03722, Korea.
Yu Seol LeeBrain Korea 21 PLUS Project for Medical Science, Yonsei University, Seoul 03722; Severance Biomedical Science Institute, Yonsei Biomedical Research Institute, Yonsei University College of Medicine, Seoul 03722, Korea.
Jin Hee KimBrain Korea 21 PLUS Project for Medical Science, Yonsei University College of Medicine, Seoul 03722, Korea.
Yejin ChoSeverance Biomedical Science Institute, Yonsei Biomedical Research Institute, Yonsei University College of Medicine, Seoul 03722, Korea.
Yoonjung JoDepartment of Bioinspired Science, Ewha Womans University, Seoul 03760, Korea.
Hyun-Seok KimDepartment of Bioinspired Science, Ewha Womans University, Seoul 03760, Korea.
Yong-Ho LeeDivision of Endocrinology and Metabolism, Department of Internal Medicine, Yonsei University College of Medicine, Seoul 03722; Institute of Endocrine Research, Yonsei University College of Medicine, Seoul 03722, Korea.
Ki Taek NamBrain Korea 21 PLUS Project for Medical Science, Yonsei University, Seoul 03722; Severance Biomedical Science Institute, Yonsei Biomedical Research Institute, Yonsei University College of Medicine, Seoul 03722, Korea.
Soo Han BaeSeverance Biomedical Science Institute, Yonsei Biomedical Research Institute, Yonsei University College of Medicine, Seoul 03722, Korea.
Yonsei University · KREwha Womans University · KRBiomedical Research Institute · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Acetaminophen (APAP) overdose can cause hepatotoxicity by inducing mitochondrial damage and subsequent necrosis in hepatocytes. Sirtuin2 (Sirt2) is an NAD+-dependent deacetylase that regulates several biological processes, including hepatic gluconeogenesis, as well as inflammatory pathways. We show that APAP decreases the expression of Sirt2. Moreover, the ablation of Sirt2 attenuates APAP-induced liver injuries, such as oxidative stress and mitochondrial damage in hepatocytes. We found that Sirt2 deficiency alleviates the APAP-mediated endoplasmic reticulum (ER) stress and phosphorylation of the p70 ribosomal S6 kinase 1 (S6K1). Moreover, Sirt2 interacts with and deacetylates S6K1, followed by S6K1 phosphorylation induction. This study elucidates the molecular mechanisms underlying the protective role of Sirt2 inactivation in APAP-induced liver injuries. [BMB Reports 2019; 52(3): 190-195].

Indexed as

AcetaminophenAnimalsChemical and Drug Induced Liver InjuryEndoplasmic Reticulum StressHepatocytesLiverMaleMiceMice, Inbred C57BLMitochondria, LiverNecrosisOxidative StressProtective AgentsRibosomal Protein S6 Kinases, 90-kDaSirtuin 2AcetaminophenProtective AgentsRibosomal Protein S6 Kinases, 90-kDaRps6ka1 protein, mouseSirt2 protein, mouseSirtuin 2

Identifiers

PMID30021675
PMCPMC6476489
OpenAlexW2929383024

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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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.