Evidence map›Paper›PMID 34405320›Full record

ArticleCell biology and toxicology2023

Induction of Sestrin2 by pterostilbene suppresses ethanol-triggered hepatocyte senescence by degrading CCN1 via p62-dependent selective autophagy.

Yiming Jiang, Ying Zhou, Wenxuan Xu, Xinqi Wang, Huanhuan Jin, Xiaofeng Bao, Chunfeng Lu

Abstract read
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In one paragraph

Article in Cell biology and toxicology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
1.1field-weighted citation impact, top 24% 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

11 citing papers in PubMed, 18 citations in OpenAlex.

  1. Review
  2. Review
  3. Article
  4. Article
  5. Review
  6. Review
  7. CCN1/Integrin αNutrients · 2022
    Article
  8. Review
  9. Article
  10. Article
  11. 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

7 authors at 3 institutions in 1 country.

Yiming Jiang *School of Pharmacy, Nantong University, 19 Qixiu Road, Nantong, 226001, Jiangsu, China.
Ying Zhou *School of Pharmacy, Nantong University, 19 Qixiu Road, Nantong, 226001, Jiangsu, China.
Wenxuan XuSchool of Pharmacy, Nanjing University of Chinese Medicine, 138 Xianlin Avenue, Nanjing, 210023, Jiangsu, China.
Xinqi WangSchool of Pharmacy, Nantong University, 19 Qixiu Road, Nantong, 226001, Jiangsu, China.
Huanhuan JinDepartment of Pharmacology, School of Pharmacy, Wannan Medical College, 22 West Wenchang Road, Wuhu, 241002, Anhui, China.
Xiaofeng BaoSchool of Pharmacy, Nantong University, 19 Qixiu Road, Nantong, 226001, Jiangsu, China.
Chunfeng LuSchool of Pharmacy, Nantong University, 19 Qixiu Road, Nantong, 226001, Jiangsu, China. ntdxlcf@ntu.edu.cn.ORCID http://orcid.org/0000-0003-3775-604X
Nantong University · CNNanjing University of Chinese Medicine · CNWannan Medical College · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Hepatocyte senescence is a key event participating in the progression of alcoholic liver disease. Autophagy is a critical biological process that controls cell fates by affecting cell behaviors like senescence. Pterostilbene is a natural compound with hepatoprotective potential; however, its implication for alcoholic liver disease was not understood. This study was aimed to investigate the therapeutic effect of pterostilbene on alcoholic liver disease and elucidate the potential mechanism. Our results showed that pterostilbene alleviated ethanol-triggered hepatocyte damage and senescence. Intriguingly, pterostilbene decreased the protein abundance of cellular communication network factor 1 (CCN1) in ethanol-exposed hepatocytes, which was essential for pterostilbene to execute its anti-senescent function. In vivo studies verified the anti-senescent effect of pterostilbene on hepatocytes of alcohol-intoxicated mice. Pterostilbene also relieved senescence-associated secretory phenotype (SASP), redox imbalance, and steatosis by suppressing hepatic CCN1 expression. Mechanistically, pterostilbene-forced CCN1 reduction was dependent on posttranscriptional regulation via autophagy machinery but not transcriptional regulation. To be specific, pterostilbene restored autophagic flux in damaged hepatocytes and activated p62-mediated selective autophagy to recognize and lead CCN1 to autolysosomes for degradation. The protein abundance of Sestrin2 (SESN2), a core upstream modulator of autophagy pathway, was decreased in ethanol-administrated hepatocytes but rescued by co-treatment with pterostilbene. Induction of SESN2 protein by pterostilbene rescued ethanol-triggered autophagic dysfunction in hepatocytes, which then reduced senescence-associated markers, postponed hepatocyte senescence, and relieved alcohol-caused liver injury and inflammation. In conclusion, this work discovered a novel compound pterostilbene with therapeutic implications for alcoholic liver disease and uncover its underlying mechanism.

Indexed as

EthanolHepatocytesAnimalsAutophagyLiverMiceStilbenesEthanolpterostilbeneStilbenesAlcoholic liver diseaseAutophagyCCN1HepatocytePterostilbeneSenescenceSestrin2

Identifiers

PMID34405320
OpenAlexW3196103792

What OpenQuestion holds

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Read underepoch 390

Registered trials

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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.