Evidence map›Paper›PMID 41175291›Full record

ReviewJournal of endocrinological investigation2026

Role of Notch signaling in corticalization.

Gherardo Mazziotti, Ernesto Canalis

Abstract readReview
In one paragraph

Review in Journal of endocrinological investigation, 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. 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

2 authors.

Gherardo MazziottiDepartment of Biomedical Sciences, Humanitas, University of Milan, Pieve Emanuele-Milan, Italy.ORCID http://orcid.org/0000-0001-5458-701X
Ernesto CanalisDepartments of Orthopaedic Surgery and Medicine UConn Musculoskeletal Institute, UConn Health, Farmington, CT, 06030, USA. canalis@uchc.edu.ORCID http://orcid.org/0000-0002-9154-952X

Funding

NIAMS NIH HHS AR072987NIAMS NIH HHS AR078149
6 · The paper itself

Abstract

Bone is a complex structure formed by cancellous and cortical bone compartments. Whereas cancellous bone remodeling has been studied extensively, less is known about mechanisms that lead to cortical bone formation and homeostasis. Corticalization is a poorly understood process, when newly formed trabeculae coalesce to consolidate as cortical bone in early life, but with an impact on skeletal integrity that is sustained throughout life. Failure to form cortical bone results in pronounced skeletal fragility, although the process is poorly understood. Mouse models of Sp7, Itgb3, Socs3 and Clcn7 inactivation exhibit impaired corticalization and cancellous bone osteopetrosis. The relationship between the two events has not been established. Notch receptors (1 through 4) are critical determinants of cell differentiation and function in the skeleton. NOTCH3 is structurally distinct and has a well-defined pattern of cellular expression, in smooth muscle vascular cells and osteocytes, conferring this Notch receptor a unique role in physiology. Mouse models expressing the biological active NOTCH3 intracellular domain (N3ICD) in Bglap

Indexed as

Bone RemodelingCortical BoneOsteogenesisReceptors, NotchSignal TransductionAnimalsHumansMiceReceptors, NotchBone fragilityCorticalizationCortical porosityFracturesOsteopetrosisTrabecularization

Identifiers

PMID41175291
PMCPMC13018096

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.