Evidence map›Paper›PMID 36825429›Full record

ArticleThe EMBO journal2023

p53 protects against alcoholic fatty liver disease via ALDH2 inhibition.

Pengbo Yao, Zhenxi Zhang, Hongchao Liu, Peng Jiang, Wei Li, Wenjing Du

Open access · greenAbstract read
In one paragraph

Article in The EMBO journal, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
5.9field-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

14 citing papers in PubMed, 23 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Article
  5. Article
  6. Genetic Polymorphisms ofInternational journal of molecular sciences · 2025
    Review
  7. Review
  8. Review
  9. [Study based on the acetaldehyde dehydrogenase 2 gene polymorphism and acetaminophen-induced liver injury].Zhonghua gan zang bing za zhi = Zhonghua ganzangbing zazhi = Chinese journal of hepatology · 2024
    Article
  10. Review
  11. Article
  12. Article
  13. Article
  14. [Nan fang yi ke da xue xue bao = Journal of Southern Medical University
    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

6 authors at 3 institutions in 1 country.

Pengbo YaoState Key Laboratory of Medical Molecular Biology, Haihe Laboratory of Cell Ecosystem, Department of Cell Biology, School of Basic Medicine Peking Union Medical College, Institute of Basic Medical Sciences Chinese Academy of Medical Sciences, Beijing, China.ORCID 0000-0003-2091-7142
Zhenxi ZhangState Key Laboratory of Medical Molecular Biology, Haihe Laboratory of Cell Ecosystem, Department of Cell Biology, School of Basic Medicine Peking Union Medical College, Institute of Basic Medical Sciences Chinese Academy of Medical Sciences, Beijing, China.
Hongchao LiuDepartment of Laboratory Medicine, Peking University Third Hospital, Beijing, China.
Peng JiangSchool of Life Sciences, Tsinghua University, Beijing, China.ORCID 0000-0002-4218-0092
Wei LiState Key Laboratory of Medical Molecular Biology, Haihe Laboratory of Cell Ecosystem, Department of Cell Biology, School of Basic Medicine Peking Union Medical College, Institute of Basic Medical Sciences Chinese Academy of Medical Sciences, Beijing, China.
Wenjing DuState Key Laboratory of Medical Molecular Biology, Haihe Laboratory of Cell Ecosystem, Department of Cell Biology, School of Basic Medicine Peking Union Medical College, Institute of Basic Medical Sciences Chinese Academy of Medical Sciences, Beijing, China.ORCID 0000-0002-9761-0774
Chinese Academy of Medical Sciences & Peking Union Medical College · CNPeking University · CNTsinghua University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The tumor suppressor p53 is critical for tumor suppression, but the regulatory role of p53 in alcohol-induced fatty liver remains unclear. Here, we show a role for p53 in regulating ethanol metabolism via acetaldehyde dehydrogenase 2 (ALDH2), a key enzyme responsible for the oxidization of alcohol. By repressing ethanol oxidization, p53 suppresses intracellular levels of acetyl-CoA and histone acetylation, leading to the inhibition of the stearoyl-CoA desaturase-1 (SCD1) gene expression. Mechanistically, p53 directly binds to ALDH2 and prevents the formation of its active tetramer and indirectly limits the production of pyruvate that promotes the activity of ALDH2. Notably, p53-deficient mice exhibit increased lipid accumulation, which can be reversed by ALDH2 depletion. Moreover, liver-specific knockdown of SCD1 alleviates ethanol-induced hepatic steatosis caused by p53 loss. By contrast, overexpression of SCD1 in liver promotes ethanol-induced fatty liver development in wild-type mice, while it has a mild effect on p53

Indexed as

Aldehyde Dehydrogenase, MitochondrialFatty LiverFatty Liver, AlcoholicTumor Suppressor Protein p53AnimalsEthanolLiverMicePyruvatesAldehyde Dehydrogenase, MitochondrialALDH2 protein, mouseEthanolPyruvatesTumor Suppressor Protein p53alcoholic fatty liverALDH2histone acetylationp53protein-protein interaction

Identifiers

PMID36825429
PMCPMC10106987
OpenAlexW4321749499

What OpenQuestion holds

Textmetadata
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.