Evidence map›Paper›PMID 34326950›Full record

ReviewWorld journal of diabetes2021

Mechanisms of altered bone remodeling in children with type 1 diabetes.

Giacomina Brunetti, Gabriele D'Amato, Stefania De Santis, Maria Grano, Maria Felicia Faienza

Open access · diamondAbstract readReview
In one paragraph

Review in World journal of diabetes, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed, 1 pooled it
2.9field-weighted citation impact, top 9% 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

20 citing papers in PubMed, 1 synthesis or guideline pooled it, 26 citations in OpenAlex.

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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

5 authors at 1 institution in 1 country.

Giacomina BrunettiDepartment of Biosciences, Biotechnologies and Biopharmaceutics, University "A. Moro" of Bari, Bari 70125, Italy. giacomina.brunetti@uniba.it.
Gabriele D'AmatoDepartment of Women's and Children's Health, ASL Bari, Neonatal Intensive Care Unit, Di Venere Hospital, Bari 70124, Italy.
Stefania De SantisDepartment of Pharmacy-Drug Science, University of Bari Aldo Moro, Bari 70126, Italy.
Maria GranoDepartment of Emergency and Organ Transplantation, Univ Bari, Bari 70124, Italy.
Maria Felicia FaienzaDepartment of Biomedical Sciences and Human Oncology, Pediatric Unit, University "A.Moro", Bari 70124, Italy.
University of Bari Aldo Moro · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Bone loss associated with type 1 diabetes mellitus (T1DM) begins at the onset of the disease, already in childhood, determining a lower bone mass peak and hence a greater risk of osteoporosis and fractures later in life. The mechanisms underlying diabetic bone fragility are not yet completely understood. Hyperglycemia and insulin deficiency can affect the bone cells functions, as well as the bone marrow fat, thus impairing the bone strength, geometry, and microarchitecture. Several factors, like insulin and growth hormone/insulin-like growth factor 1, can control bone marrow mesenchymal stem cell commitment, and the receptor activator of nuclear factor-κB ligand/osteoprotegerin and Wnt-b catenin pathways can impair bone turnover. Some myokines may have a key role in regulating metabolic control and improving bone mass in T1DM subjects. The aim of this review is to provide an overview of the current knowledge of the mechanisms underlying altered bone remodeling in children affected by T1DM.

Indexed as

Bone remodelingChildrenOsteoblastsOsteoclastsType 1 diabetes

Identifiers

PMID34326950
PMCPMC8311475
OpenAlexW3178207589

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.