Evidence map›Paper›PMID 22666632›Full record

ArticlePathology research international2012

Molecular mechanisms of liver injury and hepatocarcinogenesis: focusing on the role of stress-activated MAPK.

Hayato Nakagawa, Shin Maeda

Abstract read
In one paragraph

Article in Pathology research international, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.

0numbers the graph read from it
0cells of the map it votes in
38citing papers in PubMed
–field-weighted citation impact
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

38 citing papers in PubMed.

  1. Trial
  2. Review
  3. Hepatoprotective effects of Niudali (Food science & nutrition · 2023
    Article
  4. Article
  5. Review
  6. The mitigative effect of lotus root (Frontiers in nutrition · 2022
    Article
  7. Article
  8. Pathological predictive factors for late recurrence of hepatocellular carcinoma in chronic liver disease.Liver international : official journal of the International Association for the Study of the Liver · 2021
    Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Crosstalk between NLRP12 and JNK during Hepatocellular Carcinoma.International journal of molecular sciences · 2020
    Review
  15. Article
  16. Article
  17. Article
  18. Biosafety evaluation of Janus FeInternational journal of nanomedicine · 2018
    Article
  19. Article
  20. [Inhibitory effect of giganteaside D on hepatocellular carcinoma Hep 3b cells and the underlying mechanisms].Nan fang yi ke da xue xue bao = Journal of Southern Medical University · 2017
    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

2 authors.

Hayato NakagawaDepartment of Gastroenterology, University of Tokyo, 7-3-1 Hongo, Bunkyo-ku, Tokyo 113-8655, Japan.
Shin Maeda

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Hepatocellular carcinoma (HCC) is the third most common cause of cancer mortality. Short-term prognosis of patients with HCC has improved recently due to advances in early diagnosis and treatment, but long-term prognosis is still unsatisfactory. Therefore, obtaining a further understanding of the molecular carcinogenic mechanisms and the unique pathogenic biology of HCC is important. The most characteristic process in hepatocarcinogenesis is underlying chronic liver injury, which leads to repeated cycles of hepatocyte death, inflammation, and compensatory proliferation and subsequently provides a mitogenic and mutagenic environment leading to the development of HCC. Recent in vivo studies have shown that the stress-activated mitogen-activated protein kinase (MAPK) cascade converging on c-Jun NH(2)-terminal kinase (JNK) and p38 plays a central role in these processes, and it has attracted considerable attention as a therapeutic target. However, JNK and p38 have complex functions and a wide range of cellular effects. In addition, crosstalk with each other and the nuclear factor-kappaB pathway further complicate these functions. A full understanding is essential to bring these observations into clinical settings. In this paper, we discuss the latest findings regarding the mechanisms of liver injury and hepatocarcinogenesis focusing on the role of the stress-activated MAPK pathway.

Identifiers

PMID22666632
PMCPMC3361329

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.