Evidence map›Paper›PMID 32040707›Full record

ReviewMolecular biology reports2020

Neovascularization is a key feature of liver fibrosis progression: anti-angiogenesis as an innovative way of liver fibrosis treatment.

Mariia Zadorozhna, Sante Di Gioia, Massimo Conese, Domenica Mangieri

Abstract readReview
PubMed Publisher
In one paragraph

Review in Molecular biology reports, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed, 1 pooled it
4.5field-weighted citation impact, top 4% 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

27 citing papers in PubMed, 1 synthesis or guideline pooled it, 54 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Combining sorafenib andIranian journal of basic medical sciences · 2026
    Article
  4. Review
  5. Article
  6. Article
  7. Review
  8. Article
  9. Review
  10. Review
  11. Review
  12. Pharmacotherapy of Liver Fibrosis and Hepatitis: Recent Advances.Pharmaceuticals (Basel, Switzerland) · 2024
    Review
  13. Article
  14. Network Pharmacology and Molecular Docking Reveal the Mechanism ofDrug design, development and therapy · 2023
    Article
  15. Article
  16. ALS-L1023 fromLife (Basel, Switzerland) · 2022
    Article
  17. Article
  18. Article
  19. Article
  20. 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

4 authors at 1 institution in 1 country.

Mariia Zadorozhna *Department of Medical and Surgical Sciences, University of Foggia, Via Pinto 1, 71122, Foggia, Italy.ORCID http://orcid.org/0000-0002-4490-543X
Sante Di GioiaDepartment of Medical and Surgical Sciences, University of Foggia, Via Pinto 1, 71122, Foggia, Italy.ORCID http://orcid.org/0000-0001-7246-5622
Massimo Conese *Department of Medical and Surgical Sciences, University of Foggia, Via Pinto 1, 71122, Foggia, Italy.ORCID http://orcid.org/0000-0003-3465-6641
Domenica MangieriDepartment of Medical and Surgical Sciences, University of Foggia, Via Pinto 1, 71122, Foggia, Italy. domenica.mangieri@unifg.it.ORCID http://orcid.org/0000-0001-7350-9383
University of Foggia · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Liver fibrosis affects over 100 million people in the world; it represents a multifactorial, fibro-inflammatory disorder characterized by exacerbated production of extracellular matrix with consequent aberration of hepatic tissue. The aetiology of this disease is very complex and seems to involve a broad spectrum of factors including the lifestyle, environment factors, genes and epigenetic changes. More evidences indicate that angiogenesis, a process consisting in the formation of new blood vessels from pre-existing vessels, plays a crucial role in the progression of liver fibrosis. Central to the pathogenesis of liver fibrosis is the hepatic stellate cells (HSCs) which represent a crossroad among inflammation, fibrosis and angiogenesis. Quiescent HSCs can be stimulated by a host of growth factors, pro-inflammatory mediators produced by damaged resident liver cell types, as well as by hypoxia, contributing to neoangiogenesis, which in turn can be a bridge between acute and chronic inflammation. As matter of fact, studies demonstrated that neutralization of vascular endothelial growth factor as well as other proangiogenic agents can attenuate the progression of liver fibrosis. With this review, our intent is to discuss the cause and the role of angiogenesis in liver fibrosis focusing on the current knowledge about the impact of anti-angiogenetic therapies in this pathology.

Indexed as

Neovascularization, PathologicAngiogenesis InhibitorsAnimalsDisease ManagementDisease ProgressionDisease SusceptibilityEnvironmental BiomarkersHumansLiver CirrhosisMolecular Targeted TherapyAngiogenesis InhibitorsEnvironmental BiomarkersAngiogenesisAnti-angiogenic drugsLiver fibrosisLiver fibrosis regressionLiver information

Identifiers

PMID32040707
OpenAlexW3006434653

What OpenQuestion holds

Textmetadata
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.