Evidence map›Paper›PMID 37566009›Full record

ReviewCells2023

Glycolysis in Chronic Liver Diseases: Mechanistic Insights and Therapeutic Opportunities.

Hengdong Qu, Junli Liu, Di Zhang, Ruoyan Xie, Lijuan Wang, Jian Hong

Open access · goldAbstract readReview
In one paragraph

Review in Cells, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
6.7field-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

17 citing papers in PubMed, 31 citations in OpenAlex.

  1. Article
  2. Review
  3. Role of cellular senescence in hepatic diseases (Review).International journal of molecular medicine · 2025
    Review
  4. Review
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Review
  11. Review
  12. Article
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  14. Review
  15. Article
  16. Article
  17. Dietary Supplementation ofAquaculture nutrition · 2024
    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 1 institution in 1 country.

Hengdong QuDepartment of Pathophysiology, School of Medicine, Jinan University, Guangzhou 510632, China.
Junli LiuDepartment of Pathophysiology, School of Medicine, Jinan University, Guangzhou 510632, China.
Di ZhangDepartment of Pathophysiology, School of Medicine, Jinan University, Guangzhou 510632, China.
Ruoyan XieDepartment of Pathophysiology, School of Medicine, Jinan University, Guangzhou 510632, China.
Lijuan WangDepartment of Pathophysiology, School of Medicine, Jinan University, Guangzhou 510632, China.
Jian HongDepartment of Pathophysiology, School of Medicine, Jinan University, Guangzhou 510632, China.
Jinan University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Chronic liver diseases (CLDs) cover a spectrum of liver diseases, ranging from nonalcoholic fatty liver disease to liver cancer, representing a growing epidemic worldwide with high unmet medical needs. Glycolysis is a conservative and rigorous process that converts glucose into pyruvate and sustains cells with the energy and intermediate products required for diverse biological activities. However, abnormalities in glycolytic flux during CLD development accelerate the disease progression. Aerobic glycolysis is a hallmark of liver cancer and is responsible for a broad range of oncogenic functions including proliferation, invasion, metastasis, angiogenesis, immune escape, and drug resistance. Recently, the non-neoplastic role of aerobic glycolysis in immune activation and inflammatory disorders, especially CLD, has attracted increasing attention. Several key mediators of aerobic glycolysis, including HIF-1α and pyruvate kinase M2 (PKM2), are upregulated during steatohepatitis and liver fibrosis. The pharmacological inhibition or ablation of PKM2 effectively attenuates hepatic inflammation and CLD progression. In this review, we particularly focused on the glycolytic and non-glycolytic roles of PKM2 in the progression of CLD, highlighting the translational potential of a glycolysis-centric therapeutic approach in combating CLD.

Indexed as

Liver NeoplasmsNon-alcoholic Fatty Liver DiseaseGlycolysisHumanschronic liver diseaseglycolysisHIF-1αimmune activationmetabolic reprogrammingPKM2therapeutic target

Identifiers

PMID37566009
PMCPMC10417805
OpenAlexW4385274228

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.