Evidence map›Paper›PMID 37152902›Full record

ReviewFrontiers in molecular biosciences2023

Mechanical homeostasis imbalance in hepatic stellate cells activation and hepatic fibrosis.

Yuan-Quan Zhao, Xi-Wen Deng, Guo-Qi Xu, Jie Lin, Hua-Ze Lu, Jie Chen

Open access · goldAbstract readReview
In one paragraph

Review in Frontiers in molecular biosciences, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed, 2 pooled it
11.2field-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

33 citing papers in PubMed, 2 syntheses or guidelines pooled it, 55 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Review
  4. Review
  5. Article
  6. Detoxifying Effects of a Phenolic-RichInternational journal of molecular sciences · 2026
    Article
  7. Review
  8. Review
  9. Article
  10. Article
  11. Article
  12. Review
  13. [Causal relationship between the triglycerideZhong nan da xue xue bao. Yi xue ban = Journal of Central South University. Medical sciences · 2026
    Article
  14. Review
  15. Review
  16. Review
  17. Review
  18. 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

6 authors at 2 institutions in 1 country.

Yuan-Quan ZhaoDepartment of Hepatobiliary Surgery, Guangxi Medical University Cancer Hospital, Nanning, China.
Xi-Wen DengGraduate School of Youjiang Medical University for Nationalities, Baise, China.
Guo-Qi XuDepartment of Hepatobiliary Surgery, Guangxi Medical University Cancer Hospital, Nanning, China.
Jie LinDepartment of Hepatobiliary Surgery, Guangxi Medical University Cancer Hospital, Nanning, China.
Hua-Ze LuDepartment of Hepatobiliary Surgery, Guangxi Medical University Cancer Hospital, Nanning, China.
Jie ChenDepartment of Hepatobiliary Surgery, Guangxi Medical University Cancer Hospital, Nanning, China.
Guangxi Medical University · CNAffiliated Hospital of Youjiang Medical University for Nationalities · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Chronic liver disease or repeated damage to hepatocytes can give rise to hepatic fibrosis. Hepatic fibrosis (HF) is a pathological process of excessive sedimentation of extracellular matrix (ECM) proteins such as collagens, glycoproteins, and proteoglycans (PGs) in the hepatic parenchyma. Changes in the composition of the ECM lead to the stiffness of the matrix that destroys its inherent mechanical homeostasis, and a mechanical homeostasis imbalance activates hepatic stellate cells (HSCs) into myofibroblasts, which can overproliferate and secrete large amounts of ECM proteins. Excessive ECM proteins are gradually deposited in the Disse gap, and matrix regeneration fails, which further leads to changes in ECM components and an increase in stiffness, forming a vicious cycle. These processes promote the occurrence and development of hepatic fibrosis. In this review, the dynamic process of ECM remodeling of HF and the activation of HSCs into mechanotransduction signaling pathways for myofibroblasts to participate in HF are discussed. These mechanotransduction signaling pathways may have potential therapeutic targets for repairing or reversing fibrosis.

Indexed as

biomechanicsextracellular matrixhepatic fibrosishepatic stellate cellsmechanotransduction

Identifiers

PMID37152902
PMCPMC10157180
OpenAlexW4366549268

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.