Evidence map›Paper›PMID 35701367›Full record

ArticleJournal of cellular and molecular medicine2022

The effect of carbamazepine on bone structure and strength in control and osteogenesis imperfecta (Col1a2

Martha Blank, Narelle E McGregor, Lynn Rowley, Louise H W Kung, Blessing Crimeen-Irwin, Ingrid J Poulton, Emma C Walker, Jonathan H Gooi, Shireen R Lamandé, Natalie A Sims and 1 more

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Journal of cellular and molecular medicine, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
1.5field-weighted citation impact, top 17% 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

7 citing papers in PubMed, 8 citations in OpenAlex.

  1. Review
  2. Article
  3. Review
  4. Article
  5. Article
  6. Review
  7. 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

11 authors at 3 institutions in 1 country.

Martha BlankBone Cell Biology and Disease Unit, St. Vincent's Institute of Medical Research, Melbourne, Victoria, Australia.
Narelle E McGregorBone Cell Biology and Disease Unit, St. Vincent's Institute of Medical Research, Melbourne, Victoria, Australia.
Lynn RowleyMusculoskeletal Research, Murdoch Children's Research Institute, Melbourne, Victoria, Australia.
Louise H W KungMusculoskeletal Research, Murdoch Children's Research Institute, Melbourne, Victoria, Australia.
Blessing Crimeen-IrwinBone Cell Biology and Disease Unit, St. Vincent's Institute of Medical Research, Melbourne, Victoria, Australia.
Ingrid J PoultonBone Cell Biology and Disease Unit, St. Vincent's Institute of Medical Research, Melbourne, Victoria, Australia.
Emma C WalkerBone Cell Biology and Disease Unit, St. Vincent's Institute of Medical Research, Melbourne, Victoria, Australia.
Jonathan H GooiDepartment of Biochemistry and Molecular Biology, Bio21 Molecular Science and Biotecβhnology Institute, University of Melbourne, Parkville, Victoria, Australia.
Shireen R LamandéMusculoskeletal Research, Murdoch Children's Research Institute, Melbourne, Victoria, Australia.
Natalie A SimsBone Cell Biology and Disease Unit, St. Vincent's Institute of Medical Research, Melbourne, Victoria, Australia.
John F BatemanMusculoskeletal Research, Murdoch Children's Research Institute, Melbourne, Victoria, Australia.ORCID 0000-0001-8542-0730
The University of Melbourne · AUSt Vincents Institute of Medical Research · AUMurdoch Children's Research Institute · AU

Funding

Australian National Health & Medical Research Council GNT 1154819National Health and Medical Research Council GNT 1049863St. Vincent's InstituteVictorian Government's Operational Infrastructure Support Program
6 · The paper itself

Abstract

The inherited brittle bone disease osteogenesis imperfecta (OI) is commonly caused by COL1A1 and COL1A2 mutations that disrupt the collagen I triple helix. This causes intracellular endoplasmic reticulum (ER) retention of the misfolded collagen and can result in a pathological ER stress response. A therapeutic approach to reduce this toxic mutant load could be to stimulate mutant collagen degradation by manipulating autophagy and/or ER-associated degradation. Since carbamazepine (CBZ) both stimulates autophagy of misfolded collagen X and improves skeletal pathology in a metaphyseal chondrodysplasia model, we tested the effect of CBZ on bone structure and strength in 3-week-old male OI Col1a2

Indexed as

Osteogenesis ImperfectaAnimalsCarbamazepineCollagenCollagen Type IDisease Models, AnimalHumansMaleMiceMutationOsteogenesisX-Ray MicrotomographyCarbamazepineCOL1A2 protein, humanCollagenCollagen Type ICollagen Type I, alpha2 Subunitautophagy stimulationbiomechanicscarbamazepine treatmentdiseases and disorders of bonemicro-computed tomographyosteogenesis imperfectasynchrotron-based Fourier-transform infrared microspectroscopy

Identifiers

PMID35701367
PMCPMC9279589
OpenAlexW4282919133

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.