Evidence map›Paper›PMID 25482195›Full record

ReviewNucleus (Austin, Tex.)

Diverse lamin-dependent mechanisms interact to control chromatin dynamics. Focus on laminopathies.

Daria Camozzi, Cristina Capanni, Vittoria Cenni, Elisabetta Mattioli, Marta Columbaro, Stefano Squarzoni, Giovanna Lattanzi

Open access · goldAbstract readReview
In one paragraph

Review in Nucleus (Austin, Tex.). The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 78 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
78citing papers in PubMed, 1 pooled it
5.4field-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

78 citing papers in PubMed, 1 synthesis or guideline pooled it, 110 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Article
  4. Review
  5. Review
  6. Article
  7. 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
  8. Article
  9. Lipodystrophic Laminopathies: From Dunnigan Disease to Progeroid Syndromes.International journal of molecular sciences · 2024
    Review
  10. Article
  11. ANGPTL4 binds to the leptin receptor to regulate ectopic bone formation.Proceedings of the National Academy of Sciences of the United States of America · 2024
    Article
  12. Review
  13. Review
  14. Molecular Mechanisms for the Regulation of Nuclear Membrane Integrity.International journal of molecular sciences · 2023
    Review
  15. Review
  16. Article
  17. Article
  18. Article
  19. Review
  20. Cellular Senescence and Aging in Myotonic Dystrophy.International journal of molecular sciences · 2022
    Review

18 more citing papers are in PubMed but not listed here.

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

7 authors at 1 institution in 2 countries.

Daria Camozzia CNR Institute for Molecular Genetics; Unit of Bologna and SC Laboratory of Musculoskeletal Cell Biology; Rizzoli Orthopedic Institute; Bologna, Italy.
Cristina Capanni
Vittoria Cenni
Elisabetta Mattioli
Marta Columbaro
Stefano Squarzoni
Giovanna Lattanzi
Institute of Molecular Genetics · RU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Interconnected functional strategies govern chromatin dynamics in eukaryotic cells. In this context, A and B type lamins, the nuclear intermediate filaments, act on diverse platforms involved in tissue homeostasis. On the nuclear side, lamins elicit large scale or fine chromatin conformational changes, affect DNA damage response factors and transcription factor shuttling. On the cytoplasmic side, bridging-molecules, the LINC complex, associate with lamins to coordinate chromatin dynamics with cytoskeleton and extra-cellular signals.   Consistent with such a fine tuning, lamin mutations and/or defects in their expression or post-translational processing, as well as mutations in lamin partner genes, cause a heterogeneous group of diseases known as laminopathies. They include muscular dystrophies, cardiomyopathy, lipodystrophies, neuropathies, and progeroid syndromes. The study of chromatin dynamics under pathological conditions, which is summarized in this review, is shedding light on the complex and fascinating role of the nuclear lamina in chromatin regulation.

Indexed as

Acro-OsteolysisChromatinChromosome StructuresCytoskeletonHumansLamin Type ALamin Type BLipodystrophyLipodystrophy, Familial PartialMandibleMuscular Dystrophy, Emery-DreifussMutationNuclear EnvelopeProgeriaChromatinLamin Type ALamin Type BchromatinEmery-Dreifuss muscular dystrophyfamilial partial lipodystrophyHutchinson-Gilford progeriaLADslaminopathieslaminsmandibuloacral dysplasianuclear envelope proteins

Identifiers

PMID25482195
PMCPMC4164485
OpenAlexW2329778565

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.