Evidence map›Paper›PMID 32735894›Full record

ArticleMechanisms of ageing and development2020

A new model to investigate UVB-induced cellular senescence and pigmentation in melanocytes.

Ines Martic, Sophia Wedel, Pidder Jansen-Dürr, Maria Cavinato

Open access · hybridAbstract read
In one paragraph

Article in Mechanisms of ageing and development, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed
2.3field-weighted citation impact, top 12% 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

30 citing papers in PubMed, 47 citations in OpenAlex.

  1. Trial
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  4. Article
  5. Article
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  7. Article
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  9. Article
  10. UVB irradiation induces melanocyte damage through ferroptosis: mechanisms and implications.Photochemical & photobiological sciences : Official journal of the European Photochemistry Association and the European Society for Photobiology · 2025
    Article
  11. Telomeres in skin aging.Biogerontology · 2025
    Review
  12. Review
  13. Review
  14. Article
  15. Review
  16. Review
  17. Article
  18. Article
  19. Cutaneous Redox Senescence.Biomedicines · 2024
    Review
  20. 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

4 authors at 1 institution in 1 country.

Ines MarticInstitute for Biomedical Aging Research, Universität Innsbruck, Austria; Center for Molecular Biosciences Innsbruck (CMBI), Innsbruck, Austria.
Sophia WedelInstitute for Biomedical Aging Research, Universität Innsbruck, Austria; Center for Molecular Biosciences Innsbruck (CMBI), Innsbruck, Austria.
Pidder Jansen-DürrInstitute for Biomedical Aging Research, Universität Innsbruck, Austria; Center for Molecular Biosciences Innsbruck (CMBI), Innsbruck, Austria.
Maria CavinatoInstitute for Biomedical Aging Research, Universität Innsbruck, Austria; Center for Molecular Biosciences Innsbruck (CMBI), Innsbruck, Austria. Electronic address: maria.cavinato-nascimento@uibk.ac.at.
Universität Innsbruck · AT

Funding

Austrian Science Fund FWF P 31582
6 · The paper itself

Abstract

Ultraviolet (UV) light is known to potentially damage human skin and accelerate the skin aging process. Upon UVB exposure, melanocytes execute skin protection by increasing melanin production. Senescent cells, including senescent melanocytes, are known to accumulate in aged skin and contribute to the age-associated decline of tissue function. However, melanocyte senescence is still insufficiently explored. Here we describe a new model to investigate mechanisms of UVB-induced senescence in melanocytes and its role in photoaging. Exposure to mild and repeated doses of UVB directly influenced melanocyte proliferation, morphology and ploidy. We confirmed UVB-induced senescence with increased senescence-associated β-galactosidase positivity and changed expression of several senescence markers, including p21, p53 and Lamin B1. UVB irradiation impaired proteasome and increased autophagic activity in melanocytes, while expanding intracellular melanin content. In addition, using a co-culture system, we could confirm that senescence-associated secretory phenotype components secreted by senescent fibroblasts modulated melanogenesis. In conclusion, our new model serves as an important tool to explore UVB-induced melanocyte senescence and its involvement in photoaging and skin pigmentation.

Indexed as

Cellular SenescenceFibroblastsMelanocytesSkinAutophagybeta-GalactosidaseCell ProliferationCells, CulturedCyclin-Dependent Kinase Inhibitor p21HumansLamin Type BModels, TheoreticalProteasome Endopeptidase ComplexSkin AgingSkin PigmentationTumor Suppressor Protein p53beta-GalactosidaseCyclin-Dependent Kinase Inhibitor p21Lamin Type BProteasome Endopeptidase ComplexTumor Suppressor Protein p53MelanogenesisPigmentationProteostasisSenescenceSkin aging

Identifiers

PMID32735894
PMCPMC7116475
OpenAlexW3045782299

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.