Evidence map›Paper›PMID 35025696›Full record

ArticleAutophagy2022

Degradation of the NOTCH intracellular domain by elevated autophagy in osteoblasts promotes osteoblast differentiation and alleviates osteoporosis.

Gota Yoshida, Tsuyoshi Kawabata, Hyota Takamatsu, Shotaro Saita, Shuhei Nakamura, Keizo Nishikawa, Mari Fujiwara, Yusuke Enokidani, Tadashi Yamamuro, Keisuke Tabata and 4 more

Open access · greenAbstract read
In one paragraph

Article in Autophagy, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.

0numbers the graph read from it
0cells of the map it votes in
40citing papers in PubMed
6.7field-weighted citation impact, top 2% 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

40 citing papers in PubMed, 82 citations in OpenAlex.

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  10. The Role of Autophagy in the Mineralization Process of Bone and Dentin.International journal of molecular sciences · 2025
    Review
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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

14 authors at 3 institutions in 1 country.

Gota YoshidaDepartment of Genetics, Graduate School of Medicine, Osaka University, Osaka, Japan.
Tsuyoshi KawabataDepartment of Genetics, Graduate School of Medicine, Osaka University, Osaka, Japan.
Hyota TakamatsuDepartment of Respiratory Medicine, Allergy and Rheumatic Disease, Graduate School of Medicine, Osaka University, Osaka, Japan.
Shotaro SaitaDepartment of Genetics, Graduate School of Medicine, Osaka University, Osaka, Japan.
Shuhei NakamuraDepartment of Genetics, Graduate School of Medicine, Osaka University, Osaka, Japan.
Keizo NishikawaDepartment of Immunology and Cell Biology, Graduate School of Medicine and Frontier Biosciences, Osaka University, Osaka, Japan.
Mari FujiwaraDepartment of Genetics, Graduate School of Medicine, Osaka University, Osaka, Japan.
Yusuke EnokidaniDepartment of Genetics, Graduate School of Medicine, Osaka University, Osaka, Japan.
Tadashi YamamuroDepartment of Genetics, Graduate School of Medicine, Osaka University, Osaka, Japan.
Keisuke TabataDepartment of Genetics, Graduate School of Medicine, Osaka University, Osaka, Japan.
Maho HamasakiDepartment of Genetics, Graduate School of Medicine, Osaka University, Osaka, Japan.
Masaru IshiiDepartment of Immunology and Cell Biology, Graduate School of Medicine and Frontier Biosciences, Osaka University, Osaka, Japan.ORCID 0000-0002-4215-007X
Atsushi KumanogohDepartment of Respiratory Medicine, Allergy and Rheumatic Disease, Graduate School of Medicine, Osaka University, Osaka, Japan.
Tamotsu YoshimoriDepartment of Genetics, Graduate School of Medicine, Osaka University, Osaka, Japan.
The University of Osaka · JPDoshisha University · JPNagasaki University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Maintenance of bone integrity is mediated by the balanced actions of osteoblasts and osteoclasts. Because macroautophagy/autophagy regulates osteoblast mineralization, osteoclast differentiation, and their secretion from osteoclast cells, autophagy deficiency in osteoblasts or osteoclasts can disrupt this balance. However, it remains unclear whether upregulation of autophagy becomes beneficial for suppression of bone-associated diseases. In this study, we found that genetic upregulation of autophagy in osteoblasts facilitated bone formation. We generated mice in which autophagy was specifically upregulated in osteoblasts by deleting the gene encoding RUBCN/Rubicon, a negative regulator of autophagy. The

Indexed as

OsteogenesisOsteoporosisAlkaline PhosphataseAnimalsAutophagyBeclin-1Cell DifferentiationCore Binding Factor Alpha 1 SubunitCysteineMiceMicrotubule-Associated ProteinsOsteoblastsOsteocalcinOsteoprotegerinPhosphatesReceptors, NotchAlkaline PhosphataseBeclin-1Core Binding Factor Alpha 1 SubunitCysteineMicrotubule-Associated ProteinsOsteocalcinOsteoprotegerinPhosphatesReceptors, NotchSelective Estrogen Receptor ModulatorsSirolimusTOR Serine-Threonine KinasesBone remodelingdifferentiationmineralizationNICDosteoblastRUBCNRubicon

Identifiers

PMID35025696
PMCPMC9542956
OpenAlexW4205846964

What OpenQuestion holds

Textmetadata
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.