Evidence map›Paper›PMID 38069199›Full record

ReviewInternational journal of molecular sciences2023

Autophagy and Senescence: The Molecular Mechanisms and Implications in Liver Diseases.

Qiao Li, Yan Lin, Guangyu Liang, Nanyin Xiao, Heng Zhang, Xiao Yang, Jiankun Yang, Anding Liu

Open access · goldAbstract readReview
In one paragraph

Review in International journal of molecular sciences, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
7.7field-weighted citation impact, top 2% 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

22 citing papers in PubMed, 36 citations in OpenAlex.

  1. Article
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  7. Article
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  9. Review
  10. Review
  11. Article
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  13. Observational
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  15. Article
  16. Article
  17. Review
  18. Involvement of SIRT1-mediated aging in liver diseases.Frontiers in cell and developmental biology · 2025
    Review
  19. Review
  20. Review
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 1 institution in 1 country.

Qiao LiExperimental Medicine Center, Tongji Hospital, Tongji Medical College, Huazhong University of Sciences and Technology, Wuhan 430100, China.
Yan LinExperimental Medicine Center, Tongji Hospital, Tongji Medical College, Huazhong University of Sciences and Technology, Wuhan 430100, China.ORCID 0000-0002-3728-2027
Guangyu LiangExperimental Medicine Center, Tongji Hospital, Tongji Medical College, Huazhong University of Sciences and Technology, Wuhan 430100, China.
Nanyin XiaoExperimental Medicine Center, Tongji Hospital, Tongji Medical College, Huazhong University of Sciences and Technology, Wuhan 430100, China.
Heng ZhangExperimental Medicine Center, Tongji Hospital, Tongji Medical College, Huazhong University of Sciences and Technology, Wuhan 430100, China.
Xiao YangExperimental Medicine Center, Tongji Hospital, Tongji Medical College, Huazhong University of Sciences and Technology, Wuhan 430100, China.
Jiankun YangExperimental Medicine Center, Tongji Hospital, Tongji Medical College, Huazhong University of Sciences and Technology, Wuhan 430100, China.
Anding LiuExperimental Medicine Center, Tongji Hospital, Tongji Medical College, Huazhong University of Sciences and Technology, Wuhan 430100, China.
Tongji Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The liver is the primary organ accountable for complex physiological functions, including lipid metabolism, toxic chemical degradation, bile acid synthesis, and glucose metabolism. Liver function homeostasis is essential for the stability of bodily functions and is involved in the complex regulation of the balance between cell proliferation and cell death. Cell proliferation-halting mechanisms, including autophagy and senescence, are implicated in the development of several liver diseases, such as cholestasis, viral hepatitis, nonalcoholic fatty liver disease, liver fibrosis, and hepatocellular carcinoma. Among various cell death mechanisms, autophagy is a highly conserved and self-degradative cellular process that recycles damaged organelles, cellular debris, and proteins. This process also provides the substrate for further metabolism. A defect in the autophagy machinery can lead to premature diseases, accelerated aging, inflammatory state, tumorigenesis, and cellular senescence. Senescence, another cell death type, is an active player in eliminating premalignant cells. At the same time, senescent cells can affect the function of neighboring cells by secreting the senescence-associated secretory phenotype and induce paracrine senescence. Autophagy can promote and delay cellular senescence under different contexts. This review decodes the roles of autophagy and senescence in multiple liver diseases to achieve a better understanding of the regulatory mechanisms and implications of autophagy and senescence in various liver diseases.

Indexed as

AgingNon-alcoholic Fatty Liver DiseaseAutophagyCellular SenescenceHumansautophagyliver cancerliver fibrosisNAFLDSASPsenescence

Identifiers

PMID38069199
PMCPMC10706096
OpenAlexW4389080766

What OpenQuestion 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 OpenQuestion graph.