Evidence map›Paper›PMID 30986934›Full record

ReviewInternational journal of molecular sciences2019

LOXL2-A New Target in Antifibrogenic Therapy?

Angela Puente, Jose Ignacio Fortea, Joaquin Cabezas, Maria Teresa Arias Loste, Paula Iruzubieta, Susana Llerena, Patricia Huelin, Emilio Fábrega, Javier Crespo

Open access · goldAbstract readReview
In one paragraph

Review in International journal of molecular sciences, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.

0numbers the graph read from it
0cells of the map it votes in
39citing papers in PubMed
3.9field-weighted citation impact, top 6% 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

39 citing papers in PubMed, 78 citations in OpenAlex.

  1. Collagen in Fibrotic Diseases.Sub-cellular biochemistry · 2026
    Review
  2. Review
  3. Review
  4. Review
  5. Article
  6. Article
  7. Article
  8. Review
  9. Article
  10. Article
  11. Review
  12. Article
  13. LOXL2 in Cancer: A Two-Decade Perspective.International journal of molecular sciences · 2023
    Review
  14. Lysyl oxidase like-2 in fibrosis and cardiovascular disease.American journal of physiology. Cell physiology · 2023
    Review
  15. Dopamine Receptor D1 Is Exempt from Transforming Growth FactorThe Journal of pharmacology and experimental therapeutics · 2023
    Article
  16. Article
  17. Review
  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

9 authors at 1 institution in 1 country.

Angela PuenteDigestive Disease Department, Marqués de Valdecilla University Hospital, Cantabria University, 39008 Santander, Spain. anpuente@humv.es.
Jose Ignacio ForteaDigestive Disease Department, Marqués de Valdecilla University Hospital, Cantabria University, 39008 Santander, Spain. joseignacio.fortea@scsalud.es.
Joaquin CabezasDigestive Disease Department, Marqués de Valdecilla University Hospital, Cantabria University, 39008 Santander, Spain. joaquin.cabezas@scsalud.es.ORCID 0000-0003-0012-484X
Maria Teresa Arias LosteDigestive Disease Department, Marqués de Valdecilla University Hospital, Cantabria University, 39008 Santander, Spain. mteresa.arias@scsalud.es.
Paula IruzubietaDigestive Disease Department, Marqués de Valdecilla University Hospital, Cantabria University, 39008 Santander, Spain. paula.iruzubieta@scsalud.es.
Susana LlerenaDigestive Disease Department, Marqués de Valdecilla University Hospital, Cantabria University, 39008 Santander, Spain. susana.llerena@scsalud.es.
Patricia HuelinDigestive Disease Department, Marqués de Valdecilla University Hospital, Cantabria University, 39008 Santander, Spain. patricia.huelin@scsalud.es.
Emilio FábregaDigestive Disease Department, Marqués de Valdecilla University Hospital, Cantabria University, 39008 Santander, Spain. emilio.fabrega@scsalud.es.
Javier CrespoDigestive Disease Department, Marqués de Valdecilla University Hospital, Cantabria University, 39008 Santander, Spain. javier.crespo@scsalud.es.
Marqués de Valdecilla University Hospital · ES

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The concept of liver fibrosis and cirrhosis being static and therefore irreversible is outdated. Indeed, both human and animal studies have shown that fibrogenesis is a dynamic and potentially reversible process that can be modulated either by stopping its progression and/or by promoting its resolution. Therefore, the study of the molecular mechanisms involved in the pathogenesis of liver fibrosis is critical for the development of future antifibrotic therapies. The fibrogenesis process, common to all forms of liver injury, is characterized by the increased deposition of extracellular matrix components (EMCs), including collagen, proteoglycans, and glycoproteins (laminin and fibronectin 2). These changes in the composition of the extracellular matrix components alter their interaction with cell adhesion molecules, influencing the modulation of cell functions (growth, migration, and gene expression). Hepatic stellate cells and Kupffer cells (liver macrophages) are the key fibrogenic effectors. The antifibrogenic mechanism starts with the activation of Ly6C

Indexed as

Molecular Targeted TherapyAnimalsHumansLiver CirrhosisModels, BiologicalProtein-Lysine 6-OxidaseProtein-Lysine 6-Oxidasefibrosishepatic stellate cellsLOXL2portal hypertensionregression cirrhosis

Identifiers

PMID30986934
PMCPMC6480111
OpenAlexW2933665664

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.