Evidence map›Paper›PMID 37841641›Full record

ReviewJHEP reports : innovation in hepatology2023

Mechanobiology of portal hypertension.

Eric Felli, Sonia Selicean, Sergi Guixé-Muntet, Cong Wang, Jaume Bosch, Annalisa Berzigotti, Jordi Gracia-Sancho

Abstract readReview
In one paragraph

Review in JHEP reports : innovation in hepatology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed, 1 pooled it
–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

29 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
  2. Article
  3. Review
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Integrating mechanical cues inFrontiers in immunology · 2026
    Review
  10. Review
  11. Article
  12. Review
  13. Diagnosis of Portal Hypertension.Diagnostics (Basel, Switzerland) · 2025
    Review
  14. Article
  15. Review
  16. Review
  17. Review
  18. Review
  19. Review
  20. Blood flow-induced angiocrine signals promote organ growth and regeneration.BioEssays : news and reviews in molecular, cellular and developmental biology · 2025
    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

7 authors.

Eric FelliDepartment of Visceral Surgery and Medicine, Inselspital, Bern University Hospital, University of Bern, Switzerland.
Sonia SeliceanDepartment of Visceral Surgery and Medicine, Inselspital, Bern University Hospital, University of Bern, Switzerland.
Sergi Guixé-MuntetLiver Vascular Biology Research Group, IDIBAPS Biomedical Research Institute, CIBEREHD, Spain.
Cong WangDepartment of Visceral Surgery and Medicine, Inselspital, Bern University Hospital, University of Bern, Switzerland.
Jaume BoschDepartment of Visceral Surgery and Medicine, Inselspital, Bern University Hospital, University of Bern, Switzerland.
Annalisa BerzigottiDepartment of Visceral Surgery and Medicine, Inselspital, Bern University Hospital, University of Bern, Switzerland.
Jordi Gracia-SanchoDepartment of Visceral Surgery and Medicine, Inselspital, Bern University Hospital, University of Bern, Switzerland.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The interplay between mechanical stimuli and cellular mechanobiology orchestrates the physiology of tissues and organs in a dynamic balance characterized by constant remodelling and adaptative processes. Environmental mechanical properties can be interpreted as a complex set of information and instructions that cells read continuously, and to which they respond. In cirrhosis, chronic inflammation and injury drive liver cells dysfunction, leading to excessive extracellular matrix deposition, sinusoidal pseudocapillarization, vascular occlusion and parenchymal extinction. These pathological events result in marked remodelling of the liver microarchitecture, which is cause and result of abnormal environmental mechanical forces, triggering and sustaining the long-standing and progressive process of liver fibrosis. Multiple mechanical forces such as strain, shear stress, and hydrostatic pressure can converge at different stages of the disease until reaching a point of no return where the fibrosis is considered non-reversible. Thereafter, reciprocal communication between cells and their niches becomes the driving force for disease progression. Accumulating evidence supports the idea that, rather than being a passive consequence of fibrosis and portal hypertension (PH), mechanical force-mediated pathways could themselves represent strategic targets for novel therapeutic approaches. In this manuscript, we aim to provide a comprehensive review of the mechanobiology of PH, by furnishing an introduction on the most important mechanisms, integrating these concepts into a discussion on the pathogenesis of PH, and exploring potential therapeutic strategies.

Indexed as

hepatic stellate cellsHSCLiver cirrhosisliver fibrosisliver sinusoidal endothelial cellsLSEC

Identifiers

PMID37841641
PMCPMC10568428

What OpenQuestion holds

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Registered trials

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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.