Evidence map›Paper›PMID 32081971›Full record

ArticleScientific reports2020

CCN1 promotes hepatic steatosis and inflammation in non-alcoholic steatohepatitis.

Linling Ju, Yan Sun, Hong Xue, Lin Chen, Chunyan Gu, Jianguo Shao, Rujian Lu, Xi Luo, Jue Wei, Xiong Ma and 1 more

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
1.3field-weighted citation impact, top 20% 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

20 citing papers in PubMed, 24 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Review
  7. Cysteine-rich 61 inhibition attenuates hepatic insulin resistance and improves lipid metabolism in high-fat diet fed mice and HepG2 cells.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2024
    Article
  8. Review
  9. CCN proteins: opportunities for clinical studies-a personal perspective.Journal of cell communication and signaling · 2023
    Review
  10. Review
  11. CCN1/Integrin αNutrients · 2022
    Article
  12. Article
  13. Article
  14. Review
  15. Article
  16. Review
  17. A dietary ketone ester mitigates histological outcomes of NAFLD and markers of fibrosis in high-fat diet fed mice.American journal of physiology. Gastrointestinal and liver physiology · 2021
    Article
  18. Article
  19. Article
  20. Et tu, CCN1….Journal of cell communication and signaling · 2020
    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

11 authors at 3 institutions in 1 country.

Linling Ju *Nantong Institute of Liver Disease, Department of Gastroenterology and Hepatology, Nantong Third People's Hospital, Nantong University, Nantong, Jiangsu, China.
Yan Sun *Department of Neurology, Affiliated Hospital of Nantong University, Nantong, Jiangsu, China.
Hong XueLiver Diseases Infectious Diseases, Nantong Third People's Hospital, Nantong University, Nantong, Jiangsu, China.
Lin ChenNantong Institute of Liver Disease, Department of Gastroenterology and Hepatology, Nantong Third People's Hospital, Nantong University, Nantong, Jiangsu, China.
Chunyan GuDepartment of Pathology, Nantong Third People's Hospital, Nantong University, Nantong, Jiangsu, China.
Jianguo ShaoNantong Institute of Liver Disease, Department of Gastroenterology and Hepatology, Nantong Third People's Hospital, Nantong University, Nantong, Jiangsu, China.
Rujian LuDepartment of Cardiothoracic Surgery, Nantong Third People's Hospital, Nantong University, Nantong, Jiangsu, China.
Xi LuoNantong Institute of Liver Disease, Department of Gastroenterology and Hepatology, Nantong Third People's Hospital, Nantong University, Nantong, Jiangsu, China.
Jue WeiDepartment of Gastroenterology, Tongren Hospital, Shanghai Jiaotong University School of Medicine, Shanghai, China.
Xiong MaState Key Laboratory for Oncogenes and Related Genes, Key Laboratory of Gastroenterology & Hepatology, Ministry of Health, Division of Gastroenterology and Hepatology, Ren Ji Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai Cancer Institute, Shanghai Institute of Digestive Disease, Shanghai, China.
Zhaolian BianNantong Institute of Liver Disease, Department of Gastroenterology and Hepatology, Nantong Third People's Hospital, Nantong University, Nantong, Jiangsu, China. bianzhaolian1998@163.com.
Nantong University · CNShanghai Cancer Institute · CNTongren Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Non-alcoholic fatty liver disease (NAFLD) is characterized by increased uptake and accumulation of lipids in hepatocytes. Simple steatosis may progress to non-alcoholic steatohepatitis (NASH) with inflammation, hepatocellular injury and fibrosis. CCN1 is an important matrix protein that regulates cell death and promotes immune cell adhesion and may potentially control this process. The role of CCN1 in NASH remains unclear. We investigated the role of CCN1 in the pathogenesis of steatohepatitis. CCN1 upregulation was found to be closely related with steatosis in patients with NASH, obese mice and a FFA-treated hepatocyte model. Controlling the expression of CCN1 in murine NASH models demonstrated that CCN1 increased the severity of steatosis and inflammation. From the sequence results, we found that fatty acid metabolism genes were primarily involved in the MCD mice overexpressing CCN1 compared to the control. Then, the expression of fatty acid metabolism genes was determined using a custom-designed pathway-focused qPCR-based gene expression array. Expression analysis showed that CCN1 overexpression significantly upregulated the expression of fatty acid metabolism-associated genes. In vitro analysis revealed that CCN1 increased the intracellular TG content, the pro-inflammatory cytokines and the expression level of apoptosis-associated proteins in a steatosis model using murine primary hepatocytes. We identified CCN1 as an important positive regulator in NASH.

Indexed as

AdultAnimalsApoptosisCell AdhesionCysteine-Rich Protein 61CytokinesFatty LiverFemaleGastrointestinal DiseasesHepatocytesHumansInflammationLipid MetabolismLiverMaleMiceCCN1 protein, humanCCN1 protein, mouseCysteine-Rich Protein 61Cytokines

Identifiers

PMID32081971
PMCPMC7035350
OpenAlexW3007633187

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.