Evidence map›Paper›PMID 32456328›Full record

ReviewCells2020

Lamin A/C Mechanotransduction in Laminopathies.

Francesca Donnaloja, Federica Carnevali, Emanuela Jacchetti, Manuela Teresa Raimondi

Open access · goldAbstract readReview
In one paragraph

Review in Cells, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 papers.

0numbers the graph read from it
0cells of the map it votes in
49citing papers in PubMed
3.7field-weighted citation impact, top 6% 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

49 citing papers in PubMed, 77 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Review
  5. Review
  6. Review
  7. Article
  8. Review
  9. Article
  10. Review
  11. Article
  12. Article
  13. Review
  14. Article
  15. Review
  16. Review
  17. Article
  18. Article
  19. Article
  20. 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

4 authors at 1 institution in 1 country.

Francesca DonnalojaDepartment of Chemistry, Materials and Chemical Engineering "G.Natta", Politecnico di Milano, 20133 Milano, Italy.ORCID 0000-0001-9927-309X
Federica CarnevaliDepartment of Chemistry, Materials and Chemical Engineering "G.Natta", Politecnico di Milano, 20133 Milano, Italy.ORCID 0000-0002-0435-7272
Emanuela JacchettiDepartment of Chemistry, Materials and Chemical Engineering "G.Natta", Politecnico di Milano, 20133 Milano, Italy.ORCID 0000-0001-5990-001X
Manuela Teresa RaimondiDepartment of Chemistry, Materials and Chemical Engineering "G.Natta", Politecnico di Milano, 20133 Milano, Italy.ORCID 0000-0003-2585-7206
Politecnico di Milano · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Mechanotransduction translates forces into biological responses and regulates cell functionalities. It is implicated in several diseases, including laminopathies which are pathologies associated with mutations in lamins and lamin-associated proteins. These pathologies affect muscle, adipose, bone, nerve, and skin cells and range from muscular dystrophies to accelerated aging. Although the exact mechanisms governing laminopathies and gene expression are still not clear, a strong correlation has been found between cell functionality and nuclear behavior. New theories base on the direct effect of external force on the genome, which is indeed sensitive to the force transduced by the nuclear lamina. Nuclear lamina performs two essential functions in mechanotransduction pathway modulating the nuclear stiffness and governing the chromatin remodeling. Indeed, A-type lamin mutation and deregulation has been found to affect the nuclear response, altering several downstream cellular processes such as mitosis, chromatin organization, DNA replication-transcription, and nuclear structural integrity. In this review, we summarize the recent findings on the molecular composition and architecture of the nuclear lamina, its role in healthy cells and disease regulation. We focus on A-type lamins since this protein family is the most involved in mechanotransduction and laminopathies.

Indexed as

Mechanotransduction, CellularAnimalsHumansLaminopathiesLamin Type AMutationProtein BindingLamin Type AEmery-Dreyfuss muscular dystrophygene regulationHutchinson Gilford progeria syndromelamin A/Claminopathylamin partnersmechanotransduction

Identifiers

PMID32456328
PMCPMC7291067
OpenAlexW3027935565

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.