Evidence map›Paper›PMID 42601382›Full record

ArticleCell death and differentiation2026

PIDDosome deficiency impairs bone remodeling by increasing osteoclast ploidy and function.

M Leone, D Obwegs, N Kinz, A Maccataio, G Degenhart, R Liguori, P Y Petermann, V C Sladky, F Eichin, J S Riley and 6 more

Abstract read
PubMed Publisher
In one paragraph

Article in Cell death and differentiation, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing 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

1 citing paper in PubMed.

  1. 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

16 authors.

M LeoneInstitute for Developmental Immunology, Biocenter, Medical University of Innsbruck, Innsbruck, Austria. macileo@hotmail.com.ORCID http://orcid.org/0000-0001-6839-6265
D ObwegsInstitute for Developmental Immunology, Biocenter, Medical University of Innsbruck, Innsbruck, Austria.
N KinzInstitute for Developmental Immunology, Biocenter, Medical University of Innsbruck, Innsbruck, Austria.ORCID http://orcid.org/0009-0009-4500-2388
A MaccataioDepartment of Internal Medicine 3, Friedrich-Alexander University Erlangen-Nürnberg and Universitätsklinikum Erlangen, Erlangen, Germany.ORCID http://orcid.org/0000-0002-6814-7725
G DegenhartDepartment of Radiology, Medical University of Innsbruck, Innsbruck, Austria.ORCID http://orcid.org/0000-0002-9961-1084
R LiguoriDepartment of Nephropathology, Institute of Pathology, Friedrich-Alexander-Universität Erlangen-Nürnberg, Erlangen, Germany.
P Y PetermannInstitute for Developmental Immunology, Biocenter, Medical University of Innsbruck, Innsbruck, Austria.
V C SladkyInstitute for Developmental Immunology, Biocenter, Medical University of Innsbruck, Innsbruck, Austria.
F EichinInstitute for Developmental Immunology, Biocenter, Medical University of Innsbruck, Innsbruck, Austria.ORCID http://orcid.org/0000-0002-0085-1097
J S RileyInstitute for Developmental Immunology, Biocenter, Medical University of Innsbruck, Innsbruck, Austria.ORCID http://orcid.org/0000-0001-9170-5716
I DorigattiInstitute of Molecular Biochemistry, Biocenter, Medical University of Innsbruck, Innsbruck, Austria.ORCID http://orcid.org/0009-0000-1775-6224
K WatschingerInstitute of Molecular Biochemistry, Biocenter, Medical University of Innsbruck, Innsbruck, Austria.ORCID http://orcid.org/0000-0002-1122-8444
D RizzottoCeMM Research Center for Molecular Medicine of the Austrian Academy of Sciences, Vienna, Austria.ORCID http://orcid.org/0000-0003-0106-7496
F FerrazziDepartment of Nephropathology, Institute of Pathology, Friedrich-Alexander-Universität Erlangen-Nürnberg, Erlangen, Germany.ORCID http://orcid.org/0000-0003-4011-4638
U SteffenDepartment of Internal Medicine 3, Friedrich-Alexander University Erlangen-Nürnberg and Universitätsklinikum Erlangen, Erlangen, Germany.
A VillungerInstitute for Developmental Immunology, Biocenter, Medical University of Innsbruck, Innsbruck, Austria. andreas.villunger@i-med.ac.at.ORCID http://orcid.org/0000-0001-8259-4153

Funding

Austrian Science Fund (Fonds zur Förderung der Wissenschaftlichen Forschung) M3115Austrian Science Fund (Fonds zur Förderung der Wissenschaftlichen Forschung) P36658Deutsche Forschungsgemeinschaft (German Research Foundation) 501752319Deutsche Forschungsgemeinschaft (German Research Foundation) TRR 305-Z01Deutsche Forschungsgemeinschaft (German Research Foundation) TRR369 DIONE-B02
6 · The paper itself

Abstract

Osteoporosis is a chronic disease driven by an imbalance between bone-building osteoblasts and bone-resorbing osteoclasts, whose hyperactivation can promote this condition. Osteoclasts are multinucleated cells, and their activity directly correlates with their ploidy level. Multinucleation associates with the accumulation of extra centrosomes that can activate the PIDDosome pathway. Depending on cell type, this can lead to a p53/p21-mediated cell cycle arrest, or BCL2-regulated apoptosis. Here, we report that the PIDDosome controls polyploidization in osteoclasts and its absence triggers bone erosion in mice. PIDDosome activation in osteoclasts depends on the presence of extra centrosomes bearing the distal appendage protein ANKRD26. Consistently, loss of Ankrd26 phenocopies PIDDosome-deficiency in osteoclasts. Surprisingly, p53 and p21, which restrict cell cycle progression in the presence of extra centrosomes, are not involved in limiting osteoclast polyploidization and function. In support of this notion, bones from p53

Identifiers

PMID42601382

What OpenQuestion holds

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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.