Evidence map›Paper›PMID 31379249›Full record

ArticleAutophagy2020

Cell death induced autophagy contributes to terminal differentiation of skin and skin appendages.

Ulrich Koenig, Horst Robenek, Caterina Barresi, Marlene Brandstetter, Guenter P Resch, Marion Gröger, Thomas Pap, Christine Hartmann

Open access · hybridAbstract read
In one paragraph

Article in Autophagy, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
35citing papers in PubMed, 2 pooled it
5.3field-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

35 citing papers in PubMed, 2 syntheses or guidelines pooled it, 63 citations in OpenAlex.

  1. Pooled it
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  16. Autophagy: Regulator of cell death.Cell death & disease · 2023
    Review
  17. Article
  18. Article
  19. Autosis as a selective type of cell death.Frontiers in cell and developmental biology · 2023
    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

8 authors at 3 institutions in 2 countries.

Ulrich KoenigInstitute of Musculoskeletal Medicine, Dept. Molecular Medicine, University Hospital Münster, Westfälische Wilhelms-Universität Münster, Münster, Germany.ORCID 0000-0002-6168-8326
Horst RobenekInstitute of Musculoskeletal Medicine, Dept. Bone and Skeletal Research, University Hospital Münster, Westfälische Wilhelms-Universität Münster, Münster, Germany.
Caterina BarresiPrevious Address: Research Division of Biology and Pathobiology of the Skin, Department of Dermatology, Medical University of Vienna, Vienna, Austria.
Marlene BrandstetterElectron Microscopy Facility, Vienna Biocenter Core Facilities GmbH, Vienna, Austria.
Guenter P ReschElectron Microscopy Facility, Vienna Biocenter Core Facilities GmbH, Vienna, Austria.
Marion GrögerImaging Unit, Department of Dermatology, Medical University of Vienna, Vienna, Austria.
Thomas PapInstitute of Musculoskeletal Medicine, Dept. Molecular Medicine, University Hospital Münster, Westfälische Wilhelms-Universität Münster, Münster, Germany.
Christine HartmannInstitute of Musculoskeletal Medicine, Dept. Bone and Skeletal Research, University Hospital Münster, Westfälische Wilhelms-Universität Münster, Münster, Germany.ORCID 0000-0002-6854-8633
University of Münster · DEMedical University of Vienna · ATVienna Biocenter · AT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

In the adult mammalian skin, cells are constantly renewing, differentiating and moving upward, to finally die in a yet not fully understood manner. Here, we provide evidence that macroautophagy/autophagy has a dual role in the skin. In addition to its known catabolic protective role as an evolutionary conserved upstream regulator of lysosomal degradation, we show that autophagy induced cell death (CDA) occurs in epithelial lineage-derived organs, such as the inter-follicular epidermis, the sebaceous- and the Harderian gland. By utilizing GFP-LC3 transgenic and ATG7-deficient mice, we show that CDA is initiated during terminal differentiation at a stage when the cells have become highly resistant to apoptosis. In these transitional cells, the Golgi compartment expands, which accounts for the formation of primary lysosomes, and the nucleus starts to condense. During CDA a burst of autophagosome formation is observed, first the endoplasmic reticulum (ER) is phagocytosed followed by autophagy of the nucleus. By this selective form of cell death, most of the cytoplasmic organelles are degraded, but structural proteins remain intact. In the absence of autophagy, consequently, parts of the ER, ribosomes, and chromatin remain. A burst of autophagy was stochastically observed in single cells of the epidermis and collectively in larger areas of ductal cells, arguing for a coordinated induction. We conclude that autophagy is an integral part of cell death in keratinocyte lineage cells and participates in their terminal cell fate.

Indexed as

AnimalsApoptosisAutophagosomesAutophagyCell DifferentiationEpithelial CellsLysosomesMice, TransgenicSkinAtg7autosiscell death induced autophagy (CDA)cornificationkeratinocytesLC3lysosomesebaceous glandterminal differentiationtransmission electron microscopy (TEM)

Identifiers

PMID31379249
PMCPMC7144843
OpenAlexW2964399871

What Socratic 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 Socratic graph.