Evidence map›Paper›PMID 29854317›Full record

ReviewOncotarget2018

Lamins and bone disorders: current understanding and perspectives.

Chiara Gargiuli, Elisa Schena, Elisabetta Mattioli, Marta Columbaro, Maria Rosaria D'Apice, Giuseppe Novelli, Tiziana Greggi, Giovanna Lattanzi

Open access · diamondAbstract readReview
In one paragraph

Review in Oncotarget, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
1.4field-weighted citation impact, top 19% 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

16 citing papers in PubMed, 22 citations in OpenAlex.

  1. Article
  2. Downregulation of Nesprin1 by Runx2 deficiency is critical for the development of skeletal laminopathy-like pathology.Proceedings of the National Academy of Sciences of the United States of America · 2025
    Article
  3. Article
  4. Article
  5. Review
  6. "Bone-SASP" in Skeletal Aging.Calcified tissue international · 2023
    Review
  7. Article
  8. Components and Mechanisms of Nuclear Mechanotransduction.Annual review of cell and developmental biology · 2021
    Review
  9. From Stem Cells to Bone-Forming Cells.International journal of molecular sciences · 2021
    Review
  10. Article
  11. Article
  12. Lamin A/C and the Immune System: One Intermediate Filament, Many Faces.International journal of molecular sciences · 2020
    Review
  13. Article
  14. Article
  15. The Cutting Edge: The Role of mTOR Signaling in Laminopathies.International journal of molecular sciences · 2019
    Review
  16. Review
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

8 authors at 3 institutions in 1 country.

Chiara GargiuliCNR Institute of Molecular Genetics, Unit of Bologna, Bologna, Italy.
Elisa SchenaCNR Institute of Molecular Genetics, Unit of Bologna, Bologna, Italy.
Elisabetta MattioliCNR Institute of Molecular Genetics, Unit of Bologna, Bologna, Italy.
Marta ColumbaroRizzoli Orthopaedic Institute, Laboratory of Cell Biology, Bologna, Italy.
Maria Rosaria D'ApiceMedical Genetics Unit, Policlinico Tor Vergata University Hospital, Rome, Italy.
Giuseppe NovelliMedical Genetics Unit, Policlinico Tor Vergata University Hospital, Rome, Italy.
Tiziana GreggiRizzoli Orthopaedic Institute, Spine Deformity Department, Bologna, Italy.
Giovanna LattanziCNR Institute of Molecular Genetics, Unit of Bologna, Bologna, Italy.
Istituto Ortopedico Rizzoli · ITPoliclinico Tor Vergata · ITUniversity of Bologna · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Lamin A/C is a major constituent of the nuclear lamina implicated in a number of genetic diseases, collectively known as laminopathies. The most severe forms of laminopathies feature, among other symptoms, congenital scoliosis, osteoporosis, osteolysis or delayed cranial ossification. Importantly, specific bone districts are typically affected in laminopathies. Spine is severely affected in LMNA-linked congenital muscular dystrophy. Mandible, terminal phalanges and clavicles undergo osteolytic processes in progeroid laminopathies and Restrictive Dermopathy, a lethal developmental laminopathy. This specificity suggests that lamin A/C regulates fine mechanisms of bone turnover, as supported by data showing that lamin A/C mutations activate non-canonical pathways of osteoclastogenesis, as the one dependent on TGF beta 2. Here, we review current knowledge on laminopathies affecting bone and LMNA involvement in bone turnover and highlight lamin-dependent mechanisms causing bone disorders. This knowledge can be exploited to identify new therapeutic approaches not only for laminopathies, but also for other rare diseases featuring bone abnormalities.

Indexed as

bone turnoverhutchinson-gilford progeria syndrome (HGPS)lamin A/CLMNA-related congenital muscular dystrophy (L-CMD)mandibuloacral dysplasia (MADA, MADB)

Identifiers

PMID29854317
PMCPMC5978267
OpenAlexW2800763699

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.