Evidence map›Paper›PMID 30862117›Full record

ReviewCells2019

Deciphering Nuclear Mechanobiology in Laminopathy.

Jungwon Hah, Dong-Hwee Kim

Abstract readReview
In one paragraph

Review in Cells, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
–field-weighted citation impact
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

19 citing papers in PubMed.

  1. Review
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  14. The journal of venomous animals and toxins including tropical diseases · 2021
    Article
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  18. Review
  19. Lamin A/C promotes DNA base excision repair.Nucleic acids research · 2019
    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

2 authors.

Jungwon HahKU-KIST Graduate School of Converging Science and Technology, Korea University, Seoul 02841, Korea. jwhah@korea.ac.kr.ORCID 0000-0002-1667-0151
Dong-Hwee KimKU-KIST Graduate School of Converging Science and Technology, Korea University, Seoul 02841, Korea. donghweekim@korea.ac.kr.ORCID 0000-0003-0625-0660

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Extracellular mechanical stimuli are translated into biochemical signals inside the cell via mechanotransduction. The nucleus plays a critical role in mechanoregulation, which encompasses mechanosensing and mechanotransduction. The nuclear lamina underlying the inner nuclear membrane not only maintains the structural integrity, but also connects the cytoskeleton to the nuclear envelope. Lamin mutations, therefore, dysregulate the nuclear response, resulting in abnormal mechanoregulations, and ultimately, disease progression. Impaired mechanoregulations even induce malfunction in nuclear positioning, cell migration, mechanosensation, as well as differentiation. To know how to overcome laminopathies, we need to understand the mechanisms of laminopathies in a mechanobiological way. Recently, emerging studies have demonstrated the varying defects from lamin mutation in cellular homeostasis within mechanical surroundings. Therefore, this review summarizes recent findings highlighting the role of lamins, the architecture of nuclear lamina, and their disease relevance in the context of nuclear mechanobiology. We will also provide an overview of the differentiation of cellular mechanics in laminopathy.

Indexed as

Biophysical PhenomenaAnimalsCytoskeletonHumansLaminsMechanotransduction, CellularModels, BiologicalNuclear LaminaLaminscytoskeletonlaminlaminopathynucleus

Identifiers

PMID30862117
PMCPMC6468464

What OpenQuestion holds

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Registered trials

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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.