Evidence map›Paper›PMID 30387148›Full record

ArticleJournal of cellular physiology2019

Lysyl oxidase-like 2 is a regulator of angiogenesis through modulation of endothelial-to-mesenchymal transition.

Olivier G de Jong, Lizet M van der Waals, Farah R W Kools, Marianne C Verhaar, Bas W M van Balkom

Open access · hybridAbstract read
In one paragraph

Article in Journal of cellular physiology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
1.3field-weighted citation impact, top 19% 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

24 citing papers in PubMed, 40 citations in OpenAlex.

  1. Review
  2. Article
  3. Review
  4. Article
  5. Review
  6. Article
  7. Article
  8. LOXL2 in Cancer: A Two-Decade Perspective.International journal of molecular sciences · 2023
    Review
  9. Lysyl oxidase like-2 in fibrosis and cardiovascular disease.American journal of physiology. Cell physiology · 2023
    Review
  10. Article
  11. Article
  12. Article
  13. Article
  14. Lysyl Oxidase Family Enzymes and Their Role in Tumor Progression.International journal of molecular sciences · 2022
    Review
  15. Article
  16. Review
  17. Article
  18. LOXL2 Inhibitors and Breast Cancer Progression.Antioxidants (Basel, Switzerland) · 2021
    Review
  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

5 authors at 2 institutions in 2 countries.

Olivier G de JongDepartment of Nephrology and Hypertension, University Medical Center Utrecht, Utrecht University, Utrecht, The Netherlands.ORCID 0000-0002-5952-9617
Lizet M van der WaalsLaboratory Translational Oncology, Cancer Center, University Medical Center Utrecht, Utrecht, The Netherlands.
Farah R W KoolsDepartment of Nephrology and Hypertension, University Medical Center Utrecht, Utrecht University, Utrecht, The Netherlands.
Marianne C VerhaarDepartment of Nephrology and Hypertension, University Medical Center Utrecht, Utrecht University, Utrecht, The Netherlands.
Bas W M van BalkomDepartment of Nephrology and Hypertension, University Medical Center Utrecht, Utrecht University, Utrecht, The Netherlands.
Utrecht University · NLUniversity Medical Center Utrecht · NL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Lysyl oxidase-like 2 (LOXL2) belongs to the family of lysyl oxidases, and as such promotes crosslinking of collagens and elastin by oxidative deamination of lysine residues. In endothelial cells (ECs), LOXL2 is involved in crosslinking and scaffolding of collagen IV. Additionally, several reports have shown a role for LOXL2 in other processes, including regulation of gene expression, tumor metastasis, and epithelial-to-mesenchymal transition (EMT). Here, we demonstrate an additional role for LOXL2 in the regulation of angiogenesis by modulation of endothelial-to-mesenchymal transition (EndMT). LOXL2 knockdown in ECs results in decreased migration and sprouting, and concordantly, LOXL2 overexpression leads to an increase in migration and sprouting, independent of its catalytic activity. Furthermore, LOXL2 knockdown resulted in a reduced expression of EndMT markers, and inhibition of transforming growth factor-β (TGF-β)-mediated induction of EndMT. Interestingly, unlike in EMT, overexpression of LOXL2 alone is insufficient to induce EndMT. Further investigation revealed that LOXL2 expression regulates protein kinase B (PKB)/Akt and focal adhesion kinase (FAK) signaling, both pathways that have been implicated in the regulation of EMT. Altogether, our studies reveal a role for LOXL2 in angiogenesis through the modulation of EndMT in ECs, independent of its enzymatic crosslinking activity.

Indexed as

Epithelial-Mesenchymal TransitionNeovascularization, PhysiologicAmino Acid OxidoreductasesCell MovementCell ProliferationEndothelial CellsEnzyme ActivationFocal Adhesion Kinase 1HumansMutationProto-Oncogene Proteins c-aktSignal TransductionAmino Acid OxidoreductasesFocal Adhesion Kinase 1LOXL2 protein, humanProto-Oncogene Proteins c-aktPTK2 protein, humanangiogenesisendothelial-to-mesenchymal transitionfocal adhesion kinaselysyl oxidase-like 2protein kinase B

Identifiers

PMID30387148
PMCPMC6587725
OpenAlexW2898827765

What OpenQuestion holds

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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.