Evidence map›Paper›PMID 25008017›Full record

ReviewProgress in biophysics and molecular biology2014

Cellular mechanosensing: getting to the nucleus of it all.

Gregory R Fedorchak, Ashley Kaminski, Jan Lammerding

Abstract readReview
In one paragraph

Review in Progress in biophysics and molecular biology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 95 papers.

0numbers the graph read from it
0cells of the map it votes in
95citing 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

95 citing papers in PubMed.

  1. Review
  2. Article
  3. Review
  4. Article
  5. Article
  6. Article
  7. Review
  8. Review
  9. Article
  10. Article
  11. Principles and regulation of mechanosensing.Journal of cell science · 2024
    Review
  12. Advances in the understanding of nuclear pore complexes in human diseases.Journal of cancer research and clinical oncology · 2024
    Review
  13. Review
  14. Review
  15. Review
  16. Article
  17. Review
  18. Characterization of Breast Cancer Aggressiveness by Cell Mechanics.International journal of molecular sciences · 2023
    Article
  19. Review
  20. Article

35 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

3 authors.

Gregory R FedorchakDepartment of Biomedical Engineering, Weill Institute for Cell and Molecular Biology, Cornell University, Ithaca, NY 14853, USA.
Ashley KaminskiDepartment of Biomedical Engineering, Weill Institute for Cell and Molecular Biology, Cornell University, Ithaca, NY 14853, USA.
Jan LammerdingDepartment of Biomedical Engineering, Weill Institute for Cell and Molecular Biology, Cornell University, Ithaca, NY 14853, USA. Electronic address: jan.lammerding@cornell.edu.

Funding

TRANS-NETWORK PROJECTSU54CA143876 · NCI · CORNELL UNIVERSITY · PI SHULER, MICHAEL L · 2009 to 2014
$12.6M
Nuclear mechanics and mechanotransduction in muscular laminopathiesR01HL082792 · NHLBI · CORNELL UNIVERSITY · PI LAMMERDING, JAN · 2007 to 2023
$4.8M
Nuclear-cytoskeletal coupling in muscular laminopathiesR01NS059348 · NINDS · CORNELL UNIVERSITY · PI LAMMERDING, JAN · 2007 to 2011
$1.3M
NCI NIH HHS U54 CA143876NCI NIH HHS U54CA143876NHLBI NIH HHS R01 HL082792NINDS NIH HHS R01 NS059348NINDS NIH HHS R01 NS59348
6 · The paper itself

Abstract

Cells respond to mechanical forces by activating specific genes and signaling pathways that allow the cells to adapt to their physical environment. Examples include muscle growth in response to exercise, bone remodeling based on their mechanical load, or endothelial cells aligning under fluid shear stress. While the involved downstream signaling pathways and mechanoresponsive genes are generally well characterized, many of the molecular mechanisms of the initiating 'mechanosensing' remain still elusive. In this review, we discuss recent findings and accumulating evidence suggesting that the cell nucleus plays a crucial role in cellular mechanotransduction, including processing incoming mechanoresponsive signals and even directly responding to mechanical forces. Consequently, mutations in the involved proteins or changes in nuclear envelope composition can directly impact mechanotransduction signaling and contribute to the development and progression of a variety of human diseases, including muscular dystrophy, cancer, and the focus of this review, dilated cardiomyopathy. Improved insights into the molecular mechanisms underlying nuclear mechanotransduction, brought in part by the emergence of new technologies to study intracellular mechanics at high spatial and temporal resolution, will not only result in a better understanding of cellular mechanosensing in normal cells but may also lead to the development of novel therapies in the many diseases linked to defects in nuclear envelope proteins.

Indexed as

Models, BiologicalAnimalsCell NucleusHumansIon Channel GatingIon ChannelsMechanotransduction, CellularNuclear EnvelopeIon ChannelsCell signalingLaminsMechanicsMechanotransductionNesprinsNuclear envelope

Identifiers

PMID25008017
PMCPMC4252489

What OpenQuestion holds

Textmetadata
LicenceTDM
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.