Evidence map›Paper›PMID 31754325›Full record

ReviewInternational journal of biological sciences2019

Matrix Mechanics as Regulatory Factors and Therapeutic Targets in Hepatic Fibrosis.

Guobao Chen, Bin Xia, Qiang Fu, Xiang Huang, Fuping Wang, Zhongmin Chen, Yonggang Lv

Open access · goldAbstract readReview
In one paragraph

Review in International journal of biological sciences, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.

0numbers the graph read from it
0cells of the map it votes in
34citing papers in PubMed
5.5field-weighted citation impact, top 3% 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

34 citing papers in PubMed, 72 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Review
  5. Review
  6. Review
  7. Review
  8. Review
  9. Article
  10. Review
  11. The functional role of the extracellular matrix in inflammatory bowel disease associated gut fibrosis.Matrix biology : journal of the International Society for Matrix Biology · 2025
    Review
  12. Article
  13. Article
  14. Article
  15. Challenges ofFrontiers in cell and developmental biology · 2025
    Review
  16. Review
  17. Article
  18. Review
  19. Article
  20. MRCK as a Potential Target for Claudin-Low Subtype of Breast Cancer.International journal of biological sciences · 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

7 authors at 3 institutions in 1 country.

Guobao ChenSchool of Pharmacy and Bioengineering, Chongqing University of Technology, Chongqing 400054, P. R. China.
Bin XiaChongqing Technology and Business University, Chongqing 400067, P. R. China.
Qiang FuSchool of Pharmacy and Bioengineering, Chongqing University of Technology, Chongqing 400054, P. R. China.
Xiang HuangSchool of Pharmacy and Bioengineering, Chongqing University of Technology, Chongqing 400054, P. R. China.
Fuping WangSchool of Pharmacy and Bioengineering, Chongqing University of Technology, Chongqing 400054, P. R. China.
Zhongmin ChenSchool of Pharmacy and Bioengineering, Chongqing University of Technology, Chongqing 400054, P. R. China.
Yonggang LvKey Laboratory of Biorheological Science and Technology (Chongqing University), Ministry of Education, Bioengineering College, Chongqing University, Chongqing 400044, P. R. China.
Chongqing University of Technology · CNChongqing Technology and Business University · CNChongqing University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The hallmark of liver fibrosis is excessive extracellular matrix (ECM) synthesis and deposition that improve liver matrix remodeling and stiffening. Increased matrix stiffness is not only a pathological consequence of liver fibrosis in traditional view, but also recognized as a key driver in pathological progression of hepatic fibrosis. Cells can perceive changes in the mechanical characteristics of hepatic matrix and respond by means of mechanical signal transduction pathways to regulate cell behavior. In this review, the authors first classify causes of liver matrix stiffening during fibrotic progression, such as higher degree of collagen cross-linking. The latest advances of the research on the matrix mechanics in regulating activation of HSCs or fibroblasts under two-dimensional (2D) and three-dimensional (3D) microenvironment is also classified and summarized. The mechanical signaling pathways involved in the process of hepatic matrix stiffening, such as YAP-TAZ signaling pathway, are further summarized. Finally, some potential therapeutic concepts and strategies based on matrix mechanics will be detailed. Collectively, these findings reinforce the importance of matrix mechanics in hepatic fibrosis, and underscore the value of clarifying its modulation in hopes of advancing the development of novel therapeutic targets and strategies for hepatic fibrosis.

Indexed as

Mechanotransduction, CellularCellular MicroenvironmentCollagenDisease ProgressionExtracellular MatrixFibrosisHumansLiver DiseasesMatrix Metalloproteinase InhibitorsMatrix MetalloproteinasesSignal TransductionCollagenMatrix Metalloproteinase InhibitorsMatrix Metalloproteinaseshepatic stellate cellsliver fibrosismatrix stiffnessmechanotransductionmyofibroblaststargeting

Identifiers

PMID31754325
PMCPMC6854372
OpenAlexW2975116744

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.