Evidence map›Paper›PMID 33576035›Full record

ArticleHepatology (Baltimore, Md.)2021

Cordycepin Ameliorates Nonalcoholic Steatohepatitis by Activation of the AMP-Activated Protein Kinase Signaling Pathway.

Tian Lan, Yang Yu, Jing Zhang, Haonan Li, Qiqing Weng, Shuo Jiang, Song Tian, Tonghao Xu, Sha Hu, Guizhi Yang and 6 more

Open access · hybridAbstract read
In one paragraph

Article in Hepatology (Baltimore, Md.), 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 76 papers.

0numbers the graph read from it
0cells of the map it votes in
76citing papers in PubMed
8.1field-weighted citation impact, top 1% 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

76 citing papers in PubMed, 165 citations in OpenAlex.

  1. Article
  2. Modulation of Hepatic Cholesterol-Related Pathways byMolecules (Basel, Switzerland) · 2026
    Article
  3. Review
  4. Article
  5. Cordycepin alleviates nicotine withdrawal-induced anxietyDrug and alcohol dependence reports · 2026
    Article
  6. Article
  7. Review
  8. Review
  9. Review
  10. Article
  11. Article
  12. Article
  13. Anti-Inflammatory Mechanisms and Translational Relevance ofJournal of inflammation research · 2026
    Review
  14. Article
  15. Review
  16. Review
  17. Article
  18. Review
  19. Article
  20. Article

16 more citing papers are in PubMed but not listed here.

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.

Tian LanGuangdong Metabolic Diseases Research Center of Integrated Chinese and Western MedicineGuangdong Pharmaceutical UniversityGuangzhouChina.ORCID 0000-0002-5783-6883
Yang YuGuangdong Metabolic Diseases Research Center of Integrated Chinese and Western MedicineGuangdong Pharmaceutical UniversityGuangzhouChina.
Jing ZhangGuangdong Metabolic Diseases Research Center of Integrated Chinese and Western MedicineGuangdong Pharmaceutical UniversityGuangzhouChina.
Haonan LiGuangdong Metabolic Diseases Research Center of Integrated Chinese and Western MedicineGuangdong Pharmaceutical UniversityGuangzhouChina.
Qiqing WengGuangdong Metabolic Diseases Research Center of Integrated Chinese and Western MedicineGuangdong Pharmaceutical UniversityGuangzhouChina.
Shuo JiangGuangdong Metabolic Diseases Research Center of Integrated Chinese and Western MedicineGuangdong Pharmaceutical UniversityGuangzhouChina.
Song TianDepartment of CardiologyRenmin Hospital of Wuhan UniversityWuhanChina.
Tonghao XuGuangdong Metabolic Diseases Research Center of Integrated Chinese and Western MedicineGuangdong Pharmaceutical UniversityGuangzhouChina.
Sha HuDepartment of CardiologyRenmin Hospital of Wuhan UniversityWuhanChina.
Guizhi YangGuangdong Metabolic Diseases Research Center of Integrated Chinese and Western MedicineGuangdong Pharmaceutical UniversityGuangzhouChina.
Yan ZhangDepartment of CardiologyRenmin Hospital of Wuhan UniversityWuhanChina.
Weixuan WangGuangdong Metabolic Diseases Research Center of Integrated Chinese and Western MedicineGuangdong Pharmaceutical UniversityGuangzhouChina.
Lexun WangGuangdong Metabolic Diseases Research Center of Integrated Chinese and Western MedicineGuangdong Pharmaceutical UniversityGuangzhouChina.
Qing ZhuGuangdong Metabolic Diseases Research Center of Integrated Chinese and Western MedicineGuangdong Pharmaceutical UniversityGuangzhouChina.
Xianglu RongGuangdong Metabolic Diseases Research Center of Integrated Chinese and Western MedicineGuangdong Pharmaceutical UniversityGuangzhouChina.
Jiao GuoGuangdong Metabolic Diseases Research Center of Integrated Chinese and Western MedicineGuangdong Pharmaceutical UniversityGuangzhouChina.
Guangzhou University of Chinese Medicine · CNWuhan University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

BACKGROUND AND

aimsNonalcoholic fatty liver disease, especially nonalcoholic steatohepatitis (NASH), has become a major cause of liver transplantation and liver-associated death. NASH is the hepatic manifestation of metabolic syndrome and is characterized by hepatic steatosis, inflammation, hepatocellular injury, and different degrees of fibrosis. However, there is no US Food and Drug Administration-approved medication to treat this devastating disease. Therapeutic activators of the AMP-activated protein kinase (AMPK) have been proposed as a potential treatment for metabolic diseases such as NASH. Cordycepin, a natural product isolated from the traditional Chinese medicine Cordyceps militaris, has recently emerged as a promising drug candidate for metabolic diseases. APPROACH AND

resultsWe evaluated the effects of cordycepin on lipid storage in hepatocytes, inflammation, and fibrosis development in mice with NASH. Cordycepin attenuated lipid accumulation, inflammation, and lipotoxicity in hepatocytes subjected to metabolic stress. In addition, cordycepin treatment significantly and dose-dependently decreased the elevated levels of serum aminotransferases in mice with diet-induced NASH. Furthermore, cordycepin treatment significantly reduced hepatic triglyceride accumulation, inflammatory cell infiltration, and hepatic fibrosis in mice. In vitro and in vivo mechanistic studies revealed that a key mechanism linking the protective effects of cordycepin were AMPK phosphorylation-dependent, as indicated by the finding that treatment with the AMPK inhibitor Compound C abrogated cordycepin-induced hepatoprotection in hepatocytes and mice with NASH.

conclusionCordycepin exerts significant protective effects against hepatic steatosis, inflammation, liver injury, and fibrosis in mice under metabolic stress through activation of the AMPK signaling pathway. Cordycepin might be an AMPK activator that can be used for the treatment of NASH.

Indexed as

AMP-Activated Protein KinasesAnimalsCell LineDeoxyadenosinesHepatocytesHumansLiverLiver CirrhosisMiceNon-alcoholic Fatty Liver DiseaseSignal TransductionAMP-Activated Protein KinasescordycepinDeoxyadenosines

Identifiers

PMID33576035
PMCPMC8457150
OpenAlexW3126632176

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.