Evidence map›Paper›PMID 37752132›Full record

ArticleBone research2023

Loss of Notch signaling in skeletal stem cells enhances bone formation with aging.

Lindsey H Remark, Kevin Leclerc, Malissa Ramsukh, Ziyan Lin, Sooyeon Lee, Backialakshmi Dharmalingam, Lauren Gillinov, Vasudev V Nayak, Paulo El Parente, Margaux Sambon and 9 more

Open access · goldAbstract read
In one paragraph

Article in Bone research, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
6.2field-weighted citation impact, top 3% 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

17 citing papers in PubMed, 26 citations in OpenAlex.

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  11. Understanding the role of NOTCH2 mutation in centronuclear myopathy.Molecular therapy : the journal of the American Society of Gene Therapy · 2025
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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

19 authors at 4 institutions in 2 countries.

Lindsey H RemarkDepartment of Orthopaedic Surgery, NYU Robert I. Grossman School of Medicine, New York, NY, USA.
Kevin LeclercDepartment of Orthopaedic Surgery, NYU Robert I. Grossman School of Medicine, New York, NY, USA.
Malissa RamsukhDepartment of Orthopaedic Surgery, NYU Robert I. Grossman School of Medicine, New York, NY, USA.
Ziyan LinApplied Bioinformatics Laboratories, NYU Grossman School of Medicine, New York, NY, USA.
Sooyeon LeeDepartment of Orthopaedic Surgery, NYU Robert I. Grossman School of Medicine, New York, NY, USA.ORCID http://orcid.org/0000-0001-6244-4975
Backialakshmi DharmalingamMax Planck Institute for Molecular Biomedicine, Department of Tissue Morphogenesis, and University of Münster, Faculty of Medicine, D-48149, Münster, Germany.
Lauren GillinovDepartment of Orthopaedic Surgery, NYU Robert I. Grossman School of Medicine, New York, NY, USA.
Vasudev V NayakDepartment of Biochemistry and Molecular Biology, University of Miami Miller School of Medicine, Miami, FL, USA.
Paulo El ParenteDepartment of Orthopaedic Surgery, NYU Robert I. Grossman School of Medicine, New York, NY, USA.
Margaux SambonDepartment of Orthopaedic Surgery, NYU Robert I. Grossman School of Medicine, New York, NY, USA.
Pablo J AtriaDepartment of Orthopaedic Surgery, NYU Robert I. Grossman School of Medicine, New York, NY, USA.
Mohamed A E AliDepartment of Pathology, NYU Robert I. Grossman School of Medicine, New York, NY, USA.
Lukasz WitekBiomaterials Division, New York University College of Dentistry, New York, NY, USA.
Alesha B CastilloDepartment of Orthopaedic Surgery, NYU Robert I. Grossman School of Medicine, New York, NY, USA.
Christopher Y ParkDepartment of Pathology, NYU Robert I. Grossman School of Medicine, New York, NY, USA.
Ralf H AdamsMax Planck Institute for Molecular Biomedicine, Department of Tissue Morphogenesis, and University of Münster, Faculty of Medicine, D-48149, Münster, Germany.ORCID http://orcid.org/0000-0003-3031-7677
Aristotelis TsirigosApplied Bioinformatics Laboratories, NYU Grossman School of Medicine, New York, NY, USA.ORCID http://orcid.org/0000-0002-7512-8477
Sophie M MorganiDepartment of Orthopaedic Surgery, NYU Robert I. Grossman School of Medicine, New York, NY, USA.
Philipp LeuchtDepartment of Orthopaedic Surgery, NYU Robert I. Grossman School of Medicine, New York, NY, USA. philipp.leucht@nyulangone.org.
New York University · USUniversity of Münster · DEUniversität Ulm · DEUniversity of Miami · US

Funding

Vaccine FacilityP30CA016087 · NCI · NEW YORK UNIVERSITY SCHOOL OF MEDICINE · PI MARK Reid PHILIPS · 1985 to 2026
$83.1M
TR&D 4: Revealing Microstructure: Biophysical modeling and validation for discovery and clinical careP41EB017183 · NIBIB · NEW YORK UNIVERSITY SCHOOL OF MEDICINE · PI Daniel K Sodickson · 2014 to 2026
$19.3M
Inflamm-aging of osteoprogenitor cells: A therapeutic target for improved bone healing - Resubmission - 1 - Revision - 3R01AG056169 · NIA · NEW YORK UNIVERSITY SCHOOL OF MEDICINE · PI LEUCHT, PHILIPP · 2018 to 2022
$2.4M
Temporal balance between Notch and Wnt signaling during fracture healingK08AR069099 · NIAMS · NEW YORK UNIVERSITY SCHOOL OF MEDICINE · PI LEUCHT, PHILIPP · 2016 to 2020
$904k
Skyscan 1172 Ex-vivo MicroComputed Tomography SystemS10OD010751 · OD · NEW YORK UNIVERSITY · PI PARTRIDGE, NICOLA C · 2013 to 2013
$326k
Dissecting the Molecular Mechanisms that Govern Notch Mediated Skeletal Stem Cell Maintenance Throughout Adulthood/Aging.F30AG072834 · NIA · NEW YORK UNIVERSITY SCHOOL OF MEDICINE · PI REMARK, LINDSEY HOPE · 2022 to 2024
$158k
NCI NIH HHS P30 CA016087NIAMS NIH HHS K08 AR069099NIA NIH HHS F30 AG072834NIA NIH HHS R01 AG056169NIBIB NIH HHS P41 EB017183NIH HHS S10 OD010751
6 · The paper itself

Abstract

Skeletal stem and progenitor cells (SSPCs) perform bone maintenance and repair. With age, they produce fewer osteoblasts and more adipocytes leading to a loss of skeletal integrity. The molecular mechanisms that underlie this detrimental transformation are largely unknown. Single-cell RNA sequencing revealed that Notch signaling becomes elevated in SSPCs during aging. To examine the role of increased Notch activity, we deleted Nicastrin, an essential Notch pathway component, in SSPCs in vivo. Middle-aged conditional knockout mice displayed elevated SSPC osteo-lineage gene expression, increased trabecular bone mass, reduced bone marrow adiposity, and enhanced bone repair. Thus, Notch regulates SSPC cell fate decisions, and moderating Notch signaling ameliorates the skeletal aging phenotype, increasing bone mass even beyond that of young mice. Finally, we identified the transcription factor Ebf3 as a downstream mediator of Notch signaling in SSPCs that is dysregulated with aging, highlighting it as a promising therapeutic target to rejuvenate the aged skeleton.

Indexed as

AdipocytesOsteogenesisAdiposityAgingAnimalsArthrodesisMiceMice, KnockoutPsychomotor Agitation

Identifiers

PMID37752132
PMCPMC10522593
OpenAlexW4387036431

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.