Evidence map›Paper›PMID 32607732›Full record

ArticleHepatology international2020

Silencing of functional p53 attenuates NAFLD by promoting HMGB1-related autophagy induction.

Xuequn Zhang, Yiming Lin, Sisi Lin, Chunxiao Li, Jianguo Gao, Zemin Feng, Jinghua Wang, Jie Zhang, Hong Zhang, Yuwei Zhang and 6 more

Open access · hybridAbstract read
In one paragraph

Article in Hepatology international, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed, 1 pooled it
2.5field-weighted citation impact, top 10% 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

18 citing papers in PubMed, 1 synthesis or guideline pooled it, 24 citations in OpenAlex.

  1. Pooled it
  2. HMGB1: key mediator in digestive system diseases.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2025
    Review
  3. Article
  4. Emerging Roles of High-mobility Group Box-1 in Liver Disease.Journal of clinical and translational hepatology · 2024
    Review
  5. Review
  6. Review
  7. Review
  8. Article
  9. Review
  10. Article
  11. Protective Effects ofInternational journal of molecular sciences · 2023
    Article
  12. Review
  13. The mechanism of HMGB1 secretion and release.Experimental & molecular medicine · 2022
    Review
  14. Article
  15. Article
  16. Current Options and Future Directions for NAFLD and NASH Treatment.International journal of molecular sciences · 2021
    Review
  17. Article
  18. 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

16 authors at 2 institutions in 1 country.

Xuequn ZhangDepartment of GastroenterologyFirst Affiliated HospitalSchool of Medicine, Zhejiang University, Hangzhou, 310003, China.
Yiming LinDepartment of GastroenterologyFirst Affiliated HospitalSchool of Medicine, Zhejiang University, Hangzhou, 310003, China.
Sisi LinDepartment of Pharmacy, Zhejiang Provincial People's Hospital, Hangzhou, 310014, China.
Chunxiao LiDepartment of GastroenterologyFirst Affiliated HospitalSchool of Medicine, Zhejiang University, Hangzhou, 310003, China.
Jianguo GaoDepartment of GastroenterologyFirst Affiliated HospitalSchool of Medicine, Zhejiang University, Hangzhou, 310003, China.
Zemin FengDepartment of GastroenterologyFirst Affiliated HospitalSchool of Medicine, Zhejiang University, Hangzhou, 310003, China.
Jinghua WangDepartment of GastroenterologyFirst Affiliated HospitalSchool of Medicine, Zhejiang University, Hangzhou, 310003, China.
Jie ZhangDepartment of GastroenterologyFirst Affiliated HospitalSchool of Medicine, Zhejiang University, Hangzhou, 310003, China.
Hong ZhangDepartment of GastroenterologyFirst Affiliated HospitalSchool of Medicine, Zhejiang University, Hangzhou, 310003, China.
Yuwei ZhangDepartment of GastroenterologyFirst Affiliated HospitalSchool of Medicine, Zhejiang University, Hangzhou, 310003, China.
Xueyang ChenDepartment of GastroenterologyFirst Affiliated HospitalSchool of Medicine, Zhejiang University, Hangzhou, 310003, China.
Shenghui ChenDepartment of GastroenterologyFirst Affiliated HospitalSchool of Medicine, Zhejiang University, Hangzhou, 310003, China.
Chengfu XuDepartment of GastroenterologyFirst Affiliated HospitalSchool of Medicine, Zhejiang University, Hangzhou, 310003, China.
Youming LiDepartment of GastroenterologyFirst Affiliated HospitalSchool of Medicine, Zhejiang University, Hangzhou, 310003, China.
Chaohui YuDepartment of GastroenterologyFirst Affiliated HospitalSchool of Medicine, Zhejiang University, Hangzhou, 310003, China. zyyyych@zju.edu.cn.
Hang ZengDepartment of GastroenterologyFirst Affiliated HospitalSchool of Medicine, Zhejiang University, Hangzhou, 310003, China. zenghang@zju.edu.cn.ORCID http://orcid.org/0000-0002-3140-0125
Zhejiang University · CNZhejiang Provincial People's Hospital · CN

Funding

National key R&D Program of China 2017YFC0908901National Natural Science Foundation of China 81570523National Natural Science Foundation of China 81600457Natural Science Foundation of Zhejiang Province of China Y15H030007Zhejiang Medical and Health Science and Technology Plan Project 2014PYA008Zhejiang Medical and Health Science Research Fund 2015KYB143
6 · The paper itself

Abstract

BACKGROUND AND

aimNonalcoholic fatty liver disease (NAFLD) is a common chronic liver disease worldwide, but its pathogenesis remains imprecisely understood and requires further clarification. Recently, the tumor suppressor p53 has received growing attention for its role in metabolic diseases. In this study, we performed in vivo and in vitro experiments to identify the contribution of p53-autophagy regulation to NAFLD.

methodsLivers from wild-type and p53 knockout mice as well as p53-functional HepG2 cells and p53-dysfunctional Huh7 cells were examined for autophagy status and HMGB1 translocation. In vivo and in vitro NAFLD models were established, and steatosis was detected. In the cell models, autophagy status and steatosis were examined by p53 and/or HMGB1 silencing.

resultsFirst, the silencing of p53 could induce autophagy both in vivo and in vitro. In addition, p53 knockout attenuated high-fat diet-induced NAFLD in mice. Similarly, knockdown of p53 could alleviate palmitate-induced lipid accumulation in cell models. Furthermore, high mobility group box 1 (HMGB1) was proven to contribute to the effect of silencing p53 on alleviating NAFLD in vitro as an autophagy regulator.

conclusionThe anti-NAFLD effect of functional p53 silencing is associated with the HMGB1-mediated induction of autophagy.

Indexed as

HMGB1 ProteinLiverNon-alcoholic Fatty Liver DiseaseTumor Suppressor Protein p53AnimalsAutophagyDiet, High-FatGene SilencingHep G2 CellsHMG-Box DomainsHumansMiceHMGB1 ProteinTumor Suppressor Protein p53AutophagyHepG2High-fat dietHigh mobility group box 1Huh7MiceMouse primary hepatocytesNonalcoholic fatty liver diseasep53p62

Identifiers

PMID32607732
PMCPMC7561543
OpenAlexW3039870557

What Socratic 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 Socratic graph.