Evidence map›Paper›PMID 38761001›Full record

ArticleAging cell2024

Elimination of damaged mitochondria during UVB-induced senescence is orchestrated by NIX-dependent mitophagy.

Maria Cavinato, Ines Martic, Sophia Wedel, Annabella Pittl, Rafal Koziel, Regina Weinmmüllner, Markus Schosserer, Brigitte Jenewein, Madhusudhan Reddy Bobbili, Elsa Arcalis and 8 more

Abstract read
In one paragraph

Article in Aging cell, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
–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

20 citing papers in PubMed.

  1. Trial
  2. Article
  3. Review
  4. Review
  5. Article
  6. Review
  7. Mitochondrial regulation of cellular senescence heterogeneity.Frontiers in cell and developmental biology · 2026
    Review
  8. Review
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Review
  16. Review
  17. Autophagy-Enhancing Properties ofMolecules (Basel, Switzerland) · 2025
    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

18 authors.

Maria CavinatoInstitute for Biomedical Aging Research, University of Innsbruck, Innsbruck, Austria.ORCID 0000-0002-4891-9636
Ines MarticInstitute for Biomedical Aging Research, University of Innsbruck, Innsbruck, Austria.ORCID 0000-0002-6043-704X
Sophia WedelInstitute for Biomedical Aging Research, University of Innsbruck, Innsbruck, Austria.
Annabella PittlInstitute for Biomedical Aging Research, University of Innsbruck, Innsbruck, Austria.
Rafal KozielInstitute for Biomedical Aging Research, University of Innsbruck, Innsbruck, Austria.
Regina WeinmmüllnerInstitute of Molecular Biotechnology, University of Natural Resources and Life Sciences, Vienna, Austria.
Markus SchossererInstitute of Medical Genetics, Center for Pathobiochemistry and Genetics, Medical University Vienna, Vienna, Austria.ORCID 0000-0003-2025-0739
Brigitte JeneweinInstitute for Biomedical Aging Research, University of Innsbruck, Innsbruck, Austria.
Madhusudhan Reddy BobbiliInstitute of Molecular Biotechnology, University of Natural Resources and Life Sciences, Vienna, Austria.
Elsa ArcalisInstitut für Pflanzenbiotechnologie und Zellbiologie, University of Natural Resources and Life Sciences (BOKU), Vienna, Austria.
Johannes HaybaeckInstitute of Pathology, Neuropathology and Molecular Pathology, Medical University of Innsbruck, Innsbruck, Austria.
Gerhard PiererDepartment of Plastic, Reconstructive and Aesthetic Surgery, Medical University of Innsbruck, Innsbruck, Austria.
Christian PlonerDepartment of Plastic, Reconstructive and Aesthetic Surgery, Medical University of Innsbruck, Innsbruck, Austria.
Martin HermannDepartment of Anesthesiology and Critical Care Medicine, Medical University of Innsbruck, Innsbruck, Austria.
Nikolaus RomaniDepartment of Dermatology, Venereology and Allergology, Medical University of Innsbruck, Innsbruck, Austria.
Matthias SchmuthDepartment of Dermatology, Venereology and Allergology, Medical University of Innsbruck, Innsbruck, Austria.
Johannes GrillariInstitute of Molecular Biotechnology, University of Natural Resources and Life Sciences, Vienna, Austria.ORCID 0000-0001-5474-6332
Pidder Jansen-DürrInstitute for Biomedical Aging Research, University of Innsbruck, Innsbruck, Austria.

Funding

Austrian Science Fund FG2400BAustrian Science Fund P-315820Conselho Nacional de Desenvolvimento Científico e Tecnológico 201892/2012-0Tiroler Wissenschaftsförderung F.33287/10-2021Tiroler Wissenschaftsförderung ZAP46010University of Innsbruck
6 · The paper itself

Abstract

Skin aging is the result of two types of aging, "intrinsic aging" an inevitable consequence of physiologic and genetically determined changes and "extrinsic aging," which is dependent on external factors such as exposure to sunlight, smoking, and dietary habits. UVB causes skin injury through the generation of free radicals and other oxidative byproducts, also contributing to DNA damage. Appearance and accumulation of senescent cells in the skin are considered one of the hallmarks of aging in this tissue. Mitochondria play an important role for the development of cellular senescence, in particular stress-induced senescence of human cells. However, many aspects of mitochondrial physiology relevant to cellular senescence and extrinsic skin aging remain to be unraveled. Here, we demonstrate that mitochondria damaged by UVB irradiation of human dermal fibroblasts (HDF) are eliminated by NIX-dependent mitophagy and that this process is important for cell survival under these conditions. Additionally, UVB-irradiation of human dermal fibroblasts (HDF) induces the shedding of extracellular vesicles (EVs), and this process is significantly enhanced in UVB-irradiated NIX-depleted cells. Our findings establish NIX as the main mitophagy receptor in the process of UVB-induced senescence and suggest the release of EVs as an alternative mechanism of mitochondrial quality control in HDF.

Indexed as

Cellular SenescenceFibroblastsMitochondriaMitophagyUltraviolet RaysHumansMembrane ProteinsMitochondrial ProteinsProto-Oncogene ProteinsSkin AgingTumor Suppressor ProteinsBNIP3L protein, humanMembrane ProteinsMitochondrial ProteinsProto-Oncogene ProteinsTumor Suppressor ProteinsmitochondriamitophagyNIXsenescenceskin agingUVBvesicles

Identifiers

PMID38761001
PMCPMC11320349

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.